cell biology: cell death - volt...

Cell Biology: Cell Death

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Welcome...Key

Proteolysis

Autophagy

Proteolytic enzymes

Proteolytic inhibitors

Ubiquitination

Necrosis

Proteintech Group

ForewordBillions of cells go through the process of apoptosis – or programmed cell death – in the average human each day; it is a process of death necessary for life. The inhibition of apoptosis can result in a number of cancers, autoimmune diseases and inflammatory diseases. We have included a range of antibodies related to both extrinsic and intrinsic apoptotic pathways in this catalog. Our apoptosis signalling pathway can also be found in the centrefold (p11).

Another destructive process essential for health is autophagy. Though initially considered to be a form of non-apoptotic cell death, a consensus has emerged that autophagy, in reality, functions primarily to uphold cellular and organismal health and not exclusively cell death. You can find more about autophagy – one of cell biology’s most intriguing phenomena – in the focus articles in this catalog, including how it plays a role in cardiac health (p5) and how it may play a role in balance- sensing in mammals (p10). You can also fide a wide selection of our autophagy-related antibodies amongst these pages.As well as apoptosis, cell death can occur in several other ways such as necrosis and nerve excitotoxicity. These processes differ in nature from apoptosis and autophagy in that they are uncontrolled and lead to the lysis of cells, inflammatory responses and potentially, to serious health problems. As another important aspect of cell death, we have also included some of our antibodies relating to lytic death and proteolysis in this comprehensive selection of our cell death-related antibodies.

About UsSince our establishment in 2002 by research scientists, the team at Proteintech Group have set out to provide the research community with quality antibodies and unbeatable customer service; essentially, we strive towards a better antibody company every day. To help us achieve our goal we employ the following approaches: we make every single antibody that we sell, giving us complete control over production, quality, validation and distribution; our standard policy is to get your antibody to you the very next working day, so you can get important experiments done sooner; To top it all, we promise a guaranteed refund if you are dissatisfied with our antibodies in anyway – antibodies haven’t worked in your species or application of choice? No problem, we’ll refund the cost.

If you’re wondering how we can offer you such great terms, it’s simple; the answer lies in the science behind our antibodies. We make the majority of our antibodies using the whole protein as the antigen and purify them using antigen affinity purification; this process results in antibodies that recognize epitopes in a variety of conditions and can be used for a variety of species. As such, we are confident that you will find an antibody in our extensive catalog (catering for over 11,000 proteins!) to suit your needs – guaranteed. After all we are not satisfied unless you are; our success lies in your own.

Proteintech Group20667-1-AP

55140-1-AP

16926-1-AP

11924-1-AP

13212-1-AP

19677-1-AP

11856-1-AP

10198-1-AP

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

ELISA,WB

ELISA,WB

ELISA,WB

ELISA,WB,IHC

ELISA,WB

ELISA,WB

ELISA,WB,IHC

ELISA,WB,IHC

CAMK2D

CAMK2G

CAPS

CAPS2

CARTPT

CASP3

CASP4

CASP6

11388-1-AP Rabbit Poly ELISA,WB

CHRNA6 (AChRα6)

12250-1-AP

20558-1-AP

Rabbit Poly

Rabbit Poly

ELISA,WB,IHC

ELISA,WB

CAST

CBLN2

Stipanuk MH et al.,J Inherit Metab Dis .2011 Feb;34(1)

Recent Publications

Rabbit Poly ELISA,WB,IHC,IF

14787-1-AP

CBS20636-1-AP

20396-1-AP

20833-1-AP

60180-1-Ig

Rabbit Poly

Rabbit Poly

Rabbit Poly

Mouse Mono

ELISA,WB

ELISA,WB,IHC

ELISA,WB

ELISA,WB

CCDC115

CCDC158

CCDC42

CD34

Li YW et al.,J Hepatol .2011 Mar;54(3)Recent Publications

Rabbit Poly ELISA,WB,IHC

14486-1-AP

CD34

16669-1-AP

17617-1-AP

60181-1-Ig

21120-1-AP

12837-2-AP

12971-1-AP

16668-1-AP

10248-1-AP

10762-1-AP

13496-1-AP

10430-1-AP

13280-1-AP

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

ELISA,WB,IF

ELISA,WB,IHC

ELISA,WB

ELISA,WB

ELISA,WB,IHC

ELISA,WB

ELISA,WB,IHC

ELISA,WB

ELISA,WB

ELISA,WB

ELISA,WB

ELISA,WB

CD3D

CD3E

CD3E

CD3G

CD3ζ (ZETA)

CD40

CD40LG

CD82

CDC2

CDH23

CDK5

CEND1

Liu H et al.,Eur J Pharmacol.2011Mar 11;654(3)

Zheng S et al.,PLoS One.2011;6(6)Recent Publications


13423-1-AP

CASP8

Yang X et al.,J Proteome Res. 2010 Mar 5;9(3)

Wang WS et al.,Dis Esophagus .2010 Aug;23(6)Recent Publications


10960-1-AP

CFL1

10529-1-AP

60135-1-Ig

14968-1-AP

12527-1-AP

12048-1-AP

Rabbit Poly

Mouse Mono

Rabbit Poly

Rabbit Poly

Rabbit Poly

ELISA,WB,IHC

ELISA,WB

ELISA,WB

ELISA,WB

ELISA,WB,IHC

CHGA

CHGA

CHGB

CHMP2B

CHN1

Strunnikova NV et al.,Hum Mol Genet. 2010 Jun 15;19(12)

Recent Publications

Qian J et al.,Genes Immun .2011 Apr;12(3)Recent Publications


11553-1-AP

CHRNB1 (AChRß)

10333-1-AP

13516-1-AP

Rabbit Poly

Rabbit Poly

ELISA,WB,IHC

ELISA,WB

CHRNA3 (AChRα3)

CHRNA5 (AChRα5)

12247-1-AP

11823-1-AP

15137-1-AP

18713-1-AP

60177-1-Ig

20386-1-AP

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Mouse Mono

Rabbit Poly

ELISA,WB

ELISA,WB,IHC

ELISA,WB,IHC

ELISA,WB

ELISA,WB

ELISA,WB,IHC

CHURC1

CIB1

CKB

CKB

CKM

CLN3

V Muresan et al., J Neurosci . 2009 Mar 18;29(11)

Recent Publications

Rabbit Poly ELISA,WB

12788-1-AP

CLSTN1

21657-1-AP

21073-1-AP

10796-1-AP

12777-1-AP

10967-1-AP

18301-1-AP

12738-1-AP

14754-1-AP

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

ELISA,WB

ELISA,WB

ELISA,WB

ELISA,WB

ELISA,WB,IHC,IF

ELISA,WB

ELISA,WB

ELISA,WB,IHC,IF

CNGA3

CNN2

CNTFR

CNTN4

COIL

COL18A1

COL25A1

COMT

L Broadwater et al., Biochim Biophys Acta . 2011 May;1812(5):630-41

Recent Publications


11418-1-AP

COX5B


CPEB1

Webster MJ et al.,Int J Dev Neurosci. 2010 Oct 1

Recent Publications


10246-2-AP

CPLX1

21222-1-AP

12208-1-AP

60168-1-Ig

11211-1-AP

10317-1-AP

10317-1-AP

13474-1-AP

13997-1-AP

15808-1-AP

13760-1-AP

21009-1-AP

14388-1-AP

55027-1-AP

12245-1-AP

Rabbit Poly

Rabbit Poly

Mouse Mono

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

ELISA,WB

ELISA,WB

ELISA,WB

ELISA,WB

ELISA,WB

ELISA,WB

ELISA,WB,IF

ELISA,WB,

ELISA,WB,IHC

ELISA,WB

ELISA,WB

ELISA,WB,IF

ELISA,WB

ELISA,WB

CPLX4

CREB1 (CBP)

CRH

CRIPT

CRMP1

CRMP1

CRY1

CRY2

CRYAB

CRYBB1

CRYBB3

CSNK1D

CSPG4

CST3

Johnson SL et al.,J Neurosci .2008 Jul 23;28(30)Recent Publications


10346-1-AP

CTBP2

13974-1-AP

17565-1-AP

Rabbit Poly

Rabbit Poly

ELISA,WB,IHC,IF

ELISA,WB

CTNNA3

CTNNB1

Yao J et al.,PLoS One .2011;6(7)Recent Publications


Wei YJ et al.,Biomarkers .2008 Aug;13(5)Recent Publications


Eisenhofer G et al.,Am J Physiol Endocrinol Metab .2008 Nov;295(5)

Recent Publications


Karner CM et al.,Development .2011 Apr;138(7)

Recent Publications


14672-1-AP

15127-1-AP

10282-1-AP

20681-1-AP

14269-1-AP

15633-1-AP

13911-1-AP

19492-1-AP

10791-1-AP

17585-1-AP

10778-1-AP

17987-1-AP

55026-1-AP

16571-1-AP

10176-2-AP

60072-1-Ig

15910-1-AP

65004-1-Ig

60171-1-Ig

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Mouse Mono

Rabbit Poly

Mouse Mono

Mouse Mono

ELISA,WB,IF

ELISA,WB,IHC

ELISA,WB

ELISA,WB

ELISA,WB,IHC

ELISA,WB,IHC, IF

ELISA,WB,IHC,IF

ELISA,WB,IHC

ELISA,WB

ELISA,WB

ELISA,WB,

ELISA,WB,

ELISA,WB,IHC

ELISA,WB,IHC

ELISA,WB,

ELISA,WB,IHC

ELISA,WB,IHC

ELISA,WB

ELISA,WB

SEPT11

AAAS

AATF

ABCA2

ABCG4

ACOT2

ADAP1

ADCY3

ADD1

ADD3

ADM

ADNP

ADORA1

AHSG

AKT1

AKT1

ALDH1A1

ALDH1A1

ALDH1A1

11678-1-AP

10171-1-AP

12149-1-AP

21215-1-AP

14418-1-AP

55187-1-AP

16836-1-AP

14676-1-AP

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

ELISA,WB,IHC

ELISA,WB,IHC

ELISA,WB

ELISA,WB

ELISA,WB

ELISA,WB

ELISA,WB,IHC

ELISA,WB,IHC,IF

ARPP-19

ARRB2

ATL (SP3GA)

ATOH1

ATP1A1

ATP1A1

ATP1A2

ATP5A1

ND Amin et al., J Neurosci. 2008 Apr 2;28(14)Recent Publications

11631-1-AP Rabbit Poly ELISA,WB,IHC

12526-1-AP

13177-1-AP

19782-1-AP

11643-1-AP

12305-2-AP

15041-1-AP

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

ELISA,WB

ELISA,WB

ELISA,WB

ELISA,WB

ELISA,WB

ELISA,WB,IHC

APBB1

APBB2

APC

APH1A

APLP1

APLP2

SEPT5

13379-1-AP

AMPH

10154-2-AP

ANXA7

10520-1-AP

APOD

16290-1-AP

ARC

16608-1-AP

10524-1-AP

12639-1-AP

Rabbit Poly

Rabbit Poly

Rabbit Poly

ELISA,WB,IHC

ELISA,WB

ELISA,WB,IHCAPOF

APP (Aß42)

APPL1

ARHGAP26

ARHGEF4

ARHGEF7 (PAK7)

ARHGEF9

17747-1-AP

55213-1-AP

14092-1-AP

20042-1-AP

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

ELISA,WB

ELISA,WB

ELISA,WB

ELISA,WB

Sang L et al.,Cell .2011 May 13;145(4)Recent Publications


15693-1-AP

ATXN10

Lu CM et al.,Proteome Sci .2011 Apr 8;9(1)Recent Publications


13399-1-AP

AZGP1

A Gentilella et al., J Biol Chem , 2011 et al., 286(11):9205-15

Kettern N. et al., PLoS One , 2011;6(1)e16398Recent Publications


10599-1-AP

BAG3

Q Zi et al.,Neurochem Int et al ., 2011 Jun 11

Cui T et al., Brain Res et al., 2011 et al., 1394:1-13Recent Publications


11306-1-AP

BECN1

21776-1-AP

16541-1-AP

20540-1-AP

Rabbit Poly

Rabbit Poly

Rabbit Poly

ELISA,WB

ELISA,WB

ELISA,WBATXN2

AXIN1

AXIN2

16321-1-AP

14018-1-AP

Rabbit Poly

Rabbit Poly

ELISA,WB

ELISA,WB,IHC

BACE2

BACH1

11087-2-AP

14673-1-AP

11613-1-AP

17465-1-AP

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

ELISA,WB,IHC

ELISA,WB,IHC

ELISA,WB,IHC

ELISA,WB

BAIAP2

BAK1

BCL11A

BDNF

Morita T et al.,J Biol Chem .2009 Oct 2;284(40)Recent Publications


11589-1-AP

BRSK2

12688-1-AP

20186-1-AP

10508-1-AP

19119-1-AP

14941-1-AP

16461-1-AP

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

ELISA,WB

ELISA,WB

ELISA,WB

ELISA,WB

ELISA,WB,IHC,IF

ELISA,WB

BHLHE41

BIN3

BIRC5

BIRC5

BLMH

BPNT1

11989-1-AP

16330-1-AP

11602-1-AP

14335-1-AP

15660-1-AP

14479-1-AP

20887-1-AP

13730-1-AP

11533-1-AP

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

Rabbit Poly

ELISA,WB,IHC

ELISA,WB,IHC

ELISA,WB

ELISA,WB

ELISA,WB

ELISA,WB

ELISA,WB

ELISA,WB

ELISA,WB,IHC

BSG

BTD

C1QA

CADM1

CADM3

CALB1

CALD1

CAMK2A

CAMK2B

AAAS CTNNB1

4-5 Focus AntibodiesWe overview apoptosis and recommend some apoptosis-related antibodies, the role of GABARAPL1 in cardiac health and our cIAP1 (BIRC2) antibody.

10 Focus AntibodiesWe have an interesting article on autophagy and balance-sensing in mice.

Validation6-9 A2M-HTRRA1The first section of our cell death and degradation-related antibody selection. Published antibodies are highlighted.

Here at Proteintech we like to give you as much information as we can. This key will help you find the antibodies key to your research area:

Apoptosis

11 Signal PathwaysOur apoptosis pathway illustration can be found here too!

12-18 HTRA2-ZNF346The second section of our cell death and degradation-related antibody selection. Published antibodies are highlighted.

Proteintech Group

20667-1-AP 55140-1-AP

16926-1-AP 11924-1-AP

13212-1-AP19677-1-AP

11856-1-AP10198-1-AP

Rabbit Poly Rabbit Poly




ELISA,WB

ELISA,WB

ELISA,WB

ELISA,WB,IHC ELISA,WB

ELISA,WB

ELISA,WB,IHC ELISA,WB,IHC

CAMK2D CAMK2G

CAPS

CAPS2

CARTPT

CASP3

CASP4

CASP6


CHRNA6 (AChRα6)

12250-1-AP20558-1-AP


ELISA,WB,IHCELISA,WB

CAST

CBLN2

Stipanuk MH et al.,J Inherit Metab Dis .2011 Feb;34(1)

Recent Publications


14787-1-AP

CBS

20636-1-AP 20396-1-AP

20833-1-AP 60180-1-Ig


Rabbit PolyMouse Mono

ELISA,WB


ELISA,WB

CCDC115 CCDC158

CCDC42

CD34

Li YW et al.,J Hepatol .2011 Mar;54(3)

Recent Publications


14486-1-AP

CD34

16669-1-AP 17617-1-AP

60181-1-Ig 21120-1-AP

12837-2-AP 12971-1-AP

16668-1-AP 10248-1-AP

10762-1-AP 13496-1-AP

10430-1-AP 13280-1-AP







ELISA,WB,IFELISA,WB,IHC

ELISA,WB

ELISA,WB



ELISA,WB

ELISA,WB

ELISA,WB

ELISA,WB

CD3D

CD3E

CD3E

CD3G

CD3ζ (ZETA) CD40

CD40LG

CD82

CDC2

CDH23

CDK5

CEND1

Liu H et al.,Eur J Pharmacol.2011Mar 11;654(3)

Zheng S et al.,PLoS One.2011;6(6)

Recent Publications


13423-1-AP

CASP8

Yang X et al.,J Proteome Res. 2010 Mar 5;9(3)

Wang WS et al.,Dis Esophagus .2010 Aug;23(6)

Recent Publications


10960-1-AP

CFL1

10529-1-AP 60135-1-Ig

14968-1-AP 12527-1-AP

12048-1-AP

Rabbit PolyMouse Mono


Rabbit Poly


ELISA,WB

ELISA,WB

ELISA,WB,IHC

CHGA

CHGA

CHGB

CHMP2B

CHN1

Strunnikova NV et al.,Hum Mol Genet. 2010 Jun 15;19(12)

Recent Publications

Qian J et al.,Genes Immun .2011 Apr;12(3)

Recent Publications


11553-1-AP

CHRNB1 (AChRß)

10333-1-AP 13516-1-AP



CHRNA3 (AChRα3)

CHRNA5 (AChRα5)

12247-1-AP 11823-1-AP

15137-1-AP 18713-1-AP

60177-1-Ig 20386-1-AP



Mouse Mono Rabbit Poly

ELISA,WB

ELISA,WB,IHCELISA,WB,IHC

ELISA,WB

ELISA,WB

ELISA,WB,IHC

CHURC1

CIB1

CKB

CKB

CKM

CLN3

V Muresan et al., J Neurosci . 2009 Mar 18;29(11)

Recent Publications


12788-1-AP

CLSTN1

21657-1-AP 21073-1-AP

10796-1-AP 12777-1-AP

10967-1-AP 18301-1-AP

12738-1-AP14754-1-AP





ELISA,WB

ELISA,WB

ELISA,WB

ELISA,WB

ELISA,WB,IHC,IFELISA,WB

ELISA,WB

ELISA,WB,IHC,IF

CNGA3

CNN2

CNTFR

CNTN4

COIL

COL18A1 COL25A1

COMT

L Broadwater et al., Biochim Biophys Acta . 2011 May;1812(5):630-41

Recent Publications


11418-1-AP

COX5B


CPEB1

Webster MJ et al.,Int J Dev Neurosci. 2010 Oct 1

Recent Publications


10246-2-AP

CPLX1

21222-1-AP 12208-1-AP

60168-1-Ig 11211-1-AP

10317-1-AP 10317-1-AP

13474-1-AP 13997-1-AP

15808-1-AP 13760-1-AP

21009-1-AP 14388-1-AP

55027-1-AP 12245-1-AP


Mouse Mono Rabbit Poly






ELISA,WB

ELISA,WB

ELISA,WB

ELISA,WB

ELISA,WB

ELISA,WB

ELISA,WB,IFELISA,WB,


ELISA,WB

ELISA,WB,IFELISA,WB

ELISA,WB

CPLX4

CREB1 (CBP) CRH

CRIPT

CRMP1

CRMP1

CRY1

CRY2

CRYAB

CRYBB1

CRYBB3

CSNK1D

CSPG4

CST3

Johnson SL et al.,J Neurosci .2008 Jul 23;28(30)

Recent Publications


10346-1-AP

CTBP2

13974-1-AP 17565-1-AP



CTNNA3 CTNNB1

Yao J et al.,PLoS One .2011;6(7)

Recent Publications


Wei YJ et al.,Biomarkers .2008 Aug;13(5)

Recent Publications


Eisenhofer G et al.,Am J Physiol Endocrinol Metab .2008 Nov;295(5)

Recent Publications


Karner CM et al.,Development .2011 Apr;138(7)

Recent Publications


14672-1-AP 15127-1-AP

10282-1-AP 20681-1-AP

14269-1-AP 15633-1-AP

13911-1-AP19492-1-AP

10791-1-AP 17585-1-AP

10778-1-AP 17987-1-AP

55026-1-AP 16571-1-AP

10176-2-AP 60072-1-Ig

15910-1-AP 65004-1-Ig

60171-1-Ig








Rabbit Poly Mouse Mono

Rabbit Poly Mouse Mono

Mouse Mono

ELISA,WB,IFELISA,WB,IHC

ELISA,WB

ELISA,WB

ELISA,WB,IHC ELISA,WB,IHC, IF

ELISA,WB,IHC,IF ELISA,WB,IHC

ELISA,WB ELISA,WB

ELISA,WB,

ELISA,WB,


ELISA,WB,


ELISA,WB

ELISA,WB

SEPT11

AAAS

AATF

ABCA2

ABCG4

ACOT2

ADAP1

ADCY3

ADD1

ADD3

ADM

ADNP

ADORA1

AHSG

AKT1

AKT1

ALDH1A1 ALDH1A1

ALDH1A1

11678-1-AP 10171-1-AP

12149-1-AP 21215-1-AP

14418-1-AP 55187-1-AP

16836-1-AP14676-1-AP






ELISA,WB

ELISA,WB

ELISA,WB

ELISA,WB

ELISA,WB,IHCELISA,WB,IHC,IF

ARPP-19

ARRB2

ATL (SP3GA) ATOH1

ATP1A1

ATP1A1

ATP1A2

ATP5A1

ND Amin et al., J Neurosci. 2008 Apr 2;28(14)

Recent Publications

11631-1-AP Rabbit Poly ELISA,WB,IHC

12526-1-AP13177-1-AP

19782-1-AP 11643-1-AP

12305-2-AP15041-1-AP




ELISA,WB

ELISA,WB

ELISA,WB

ELISA,WB

ELISA,WB

ELISA,WB,IHC

APBB1

APBB2

APC

APH1A

APLP1

APLP2

SEPT5

13379-1-AP

AMPH

10154-2-AP

ANXA7

10520-1-AP

APOD

16290-1-AP

ARC

16608-1-AP 10524-1-AP

12639-1-AP


Rabbit Poly


ELISA,WB,IHC

APOF

APP (Aß42) APPL1

ARHGAP26 ARHGEF4

ARHGEF7 (PAK7)ARHGEF9

17747-1-AP 55213-1-AP

14092-1-AP20042-1-AP



ELISA,WB

ELISA,WB

ELISA,WB

ELISA,WB

Sang L et al.,Cell .2011 May 13;145(4)

Recent Publications


15693-1-AP

ATXN10

Lu CM et al.,Proteome Sci .2011 Apr 8;9(1)

Recent Publications


13399-1-AP

AZGP1

A Gentilella et al., J Biol Chem , 2011 et al., 286(11):9205-15

Kettern N. et al., PLoS One , 2011;6(1)e16398

Recent Publications


10599-1-AP

BAG3

Q Zi et al.,Neurochem Int et al ., 2011 Jun 11

Cui T et al., Brain Res et al., 2011 et al., 1394:1-13

Recent Publications


11306-1-AP

BECN1

21776-1-AP 16541-1-AP

20540-1-AP


Rabbit Poly

ELISA,WB

ELISA,WB

ELISA,WB

ATXN2

AXIN1

AXIN2

16321-1-AP 14018-1-AP


ELISA,WB

ELISA,WB,IHC

BACE2

BACH1

11087-2-AP 14673-1-AP

11613-1-AP 17465-1-AP





BAIAP2

BAK1

BCL11A

BDNF

Morita T et al.,J Biol Chem .2009 Oct 2;284(40)

Recent Publications


11589-1-AP

BRSK2

12688-1-AP 20186-1-AP

10508-1-AP 19119-1-AP

14941-1-AP16461-1-AP




ELISA,WB

ELISA,WB

ELISA,WB

ELISA,WB


BHLHE41 BIN3

BIRC5

BIRC5

BLMH

BPNT1

11989-1-AP 16330-1-AP

11602-1-AP 14335-1-AP

15660-1-AP 14479-1-AP

20887-1-AP13730-1-AP

11533-1-AP





Rabbit Poly


ELISA,WB

ELISA,WB

ELISA,WB

ELISA,WB

ELISA,WB

ELISA,WB

ELISA,WB,IHC

BSG

BTD

C1QA

CADM1

CADM3

CALB1

CALD1

CAMK2A

CAMK2B

AAAS CTNNB1

Cleavage of

caspase substrates

DNA

Survival

Genes

Degradation

Intrinsic

Pathway

Stress Signals

DNA

Death

genes

MITOCHONDRIA

Survival

Factors

Ca2+- induced

Cell Death Pathways

Extrinsic Pathway

Death Ligand

Apoptosis, derived from the Greek word for “falling off” or “dropping

off” (like leaves from a tree), is defined by distinct morphological

and biochemical changes. These changes are mediated by a family

of cysteine aspartic acid-specific proteases (caspases), which are

expressed as inactive precursors or zymogens (pro-caspases) and

are proteolytically processed to an active state following an apoptotic

stimulus. To date, 14 mammalian caspases have been identified and

these can be roughly divided into three functional groups: apoptosis

initiators (including caspase-2, -9, -8, -10), apoptosis effectors

(including caspase-3, -6, -7), and cytokine maturation caspases

(including caspase-1, -4, -5, -11, -12, -13, -14).

Apoptosis

Signaling Pathway

For more information on all the antibodies featured here or to view

our extensive catalog, visit www.ptglab.com

Proteintech Group

Focus Antibodies

Apoptosis, derived from the Greek word for “falling off” or “dropping off”, is defined by distinct morphological and biochemical changes in the cell. These changes are mediated by a family of cysteine aspartic acid-specific proteases or caspases, which are expressed as inactive precursors or zymogens (pro-caspases) and are proteolytically processed to an active state following an apoptotic stimulus. To date, 14 mammalian caspases have been identified and these can be roughly divided into three functional groups: apoptosis initiators (including caspase-2, -9, -8 and -10), apoptosis effectors (including caspase-3, -6 and -7), and cytokine maturation caspases (including caspase-1, -4, -5, -11, -12, -13 and -14).

Extrinsic pathwayCaspases may be activated by an extrinsic pathway or by an intrinsic pathway. The extrinsic pathway is initiated by the binding of transmembrane death receptors (Fas, TNF receptor, and TRAIL receptor) with their respective ligands (FasL, TNF, and TRAIL) to activate membrane-

proximal caspases (caspase-8 and -10), which in turn cleave and activate effector caspases such as caspase-3 and -7. This pathway can be regulated by FLIP, which inhibits upstream initiator caspases, and inhibitor of apoptosis proteins (IAPs), which affect both initiator and effector caspases.

Intrinsic pathway – the role of mitochondriaThe intrinsic pathway requires disruption of the mitochondrial membrane and the release of mitochondrial proteins, such as cytochrome c. Cytochrome c released from the mitochondrial intermembrane space into the cytoplasm, works together with the other two cytosolic protein factors, Apaf-1 (apoptotic protease activating factor-1) and procaspase-9, to promote the assembly of a caspase-activating complex termed the apoptosome, which in return induces activation of caspase-9 and thereby initiates the apoptotic caspase cascade.

Control of cytochrome c releaseThe primary regulatory step for mitochondrial-mediated caspase activation (the intrinsic pathway) is at the level of cytochrome c release. The known regulators of cytochrome c release are the Bcl-2 family proteins. The mammalian Bcl-2 family can be divided into pro-apoptotic and anti-apoptotic members. The pro-apoptotic members include Bax and Bad. The anti-apoptotic Bcl-2 family members include Bcl-2 and Bcl-XL. Overexpression of the anti-apoptotic molecules blocks cytochrome c release in response to a variety of apoptotic stimuli. On the contrary, the pro- apoptotic members of the Bcl-2 family proteins promote cytochrome c release from the mitochondria.

Cross-talkThere is considerable cross-talk between the extrinsic and intrinsic pathways. For example, caspase- 8 can proteolytically activate Bid, which then facilitates the release of cytochrome c and amplifies the apoptotic signal following death receptor activation. Most anticancer agents either directly induce DNA damage or indirectly induce secondary stress-responsive signaling pathways to trigger

Keywords: apoptosis, Bcl, caspase, CytC, extrinsic pathway, FADD, FAS, FLIP, intrinsic pathway, TRAIL

apoptosis by activation of the intrinsic apoptotic pathway, and some can simultaneously activate the extrinsic receptor pathway.

Apoptosis and chemotherapyMost chemotherapeutic drugs kill cancer cells by inducing apoptosis, and many similarities exist in cellular response to drug-induced apoptosis, regardless of their primary target. Defects in apoptosis signaling commonly contribute to the resistance of tumors to chemotherapy.

Proteintech stock a wide range of apoptosis-related antibodies and are adding more to our catalog all the time, browse the catalog for more of our apoptosis related antibodies.

Apoptosis – The Basics

Related Antibodies:

cIAP2 (BIRC3)

CASP2 CASP3 CASP9 TRAILR4

CASP2 CASP3 CASP4 CASP6CASP8 CASP9 CASP10 CASP12 cIAP1 (BIRC2) cIAP2 (BIRC3) FASFAS TNFR1 TRAIL TRAIL TRAILR4 TRAILR2

rabbit polyclonal: rabbit polyclonal: rabbit polyclonal: rabbit polyclonal: rabbit polyclonal: rabbit polyclonal: rabbit polyclonal: rabbit polyclonal: rabbit polyclonal: rabbit polyclonal:rabbit polyclonal: mouse monoclonal:rabbit polyclonal: rabbit polyclonal: rabbit polyclonal: rabbit polyclonal: mouse monoclonal:

10436-1-AP19677-1-AP11856-1-AP10198-1-AP13423-1-AP10380-1-AP 14311-1-AP 55238-1-AP 10022-1-AP10058-1-AP 13098-1-AP60196-1-Ig 21574-1-AP 10399-1-AP 17235-1-AP 16781-1-AP 65046-1-Ig

Published antibodies.Here are some of our cell death related antibodies:Look out for the to quickly find all of our published antibodies

Turn the page to browse a selection of cell death related antibodies.

The inhibitor of apoptosis proteins (IAPs) are a family of anti-apoptotic regulators found in viruses and metazoans. c-IAP1 (10022-1-AP) and c-IAP2 (10058-1-AP) are recruited to tumor necrosis factor receptor (TNFR) 1-associated complexes, such as activated CD40 receptors (12971-1-AP), where they can regulate receptor-mediated signaling and the degradation of TNFR associated factors (TRAFs). CD40 is a member of the TNFR superfamily and is responsible for the efficient activation of cell- mediated and humoral immune responses via activated T cells and B cells respectively.

Our c-IAP1 antibody has featured in various publications investigating CD40 signaling [1-2] FAS- mediated apoptosis in human leukemia T-cells [3] and NFκB activation [2-3]. The most recent paper [1], published in the Journal of

Immunology last year, looks into the signaling properties of a variant form of human CD40 receptor. Authors Anna Peters and Gail Bishop had previously identified this as a gain-of-function allele producing a proline-to-alanine amino acid substitution at position 227 of CD40 (hCD40-P227A). In the current study the authors show that hCD40-P227A binds more TRAF3 (amongst other associated proteins) than wild-type CD40, yet both forms of the receptor bind similar amounts of cIAP1. As a result of higher TRAF3 binding, CD40 signalling changes dramatically causing hyperactivity of the JNK stress/inflammatory response pathway.

Autophagy is a pathway for the degradation and recycling of long-lived proteins and cytoplasmic organelles through the lysosome and plays an important role in homeostasis and cell survival. It is required for normal cardiac function and has also been implicated in cardiovascular disease. Two recent publications have investigated autophagy in cardiomyocytes and the Proteintech GABARAPL1 rabbit polyclonal antibody has played a key role in this work.

The GABA (A) receptor-associated protein-like 1 (GABARA-PL1) was first described as an estrogen regulated gene which shares a high sequence homology with the gabarap gene. It interacts with the GABAA receptor and tubulin and promotes tubulin polymerization. Previous work has demonstrated that the GABARAP family members (GABARAP, LC3, GATE-16 and Atg8) are not only involved in the transport of proteins or vesicles but are also implicated in various mechanisms such cell death, cell proliferation and autophagy; during autophagy GABARAPL1 associates with autophagic vesicles and is a useful marker of the autophagic process. These properties of GABARAPL1 have recently been utilized in the study of autophagy in cardiomyocytes.

FoxO induces GABARAPL1 expressionKatherine Yutzey’s team at the Cincinnati Children’s Medical Center, Ohio, US investigated the role of the FoxO transcrip-tion factor in regulating autophagy and cell size in cardio-myocytes. They report that FoxO overexpression reduces cardiomyocyte cell size and induces expression of autophagy pathway markers such as GABARAPL1 and ATG12. Induction

of GABARAPL1 expression was shown by confocal micros-copy. They also found that FoxO was directly responsible for GABARAPL1 induction, as the GABRAPL1 promoter was identified as a FoxO binding site through chromatin immuno-precipitation (ChIP) experiments [1].

Down-regulation of autophagy after mechanical unloading in heartKassiotis et al, report in Circulation that markers of autophagy are down-regulated in failing human hearts after mechanical unloading. Mechanical unloading involves a medical device assisting the heart and means a decreased energy demand from the failing heart. The researchers found that protein expression levels of GABARAPL1, ATG5 and ATG12 were all reduced under mechanical loading conditions, as measured by quantitative western blotting. The authors suggest that au-tophagy may be an adaptive mechanism in the failing heart and that this phenomenon is attenuated by mechanical unloading [2].

Cardiac autophagy and GABARAPL1

Keywords: apoptosis, Bcl, caspase, CytC, extrinsic pathway, FADD, FAS, FLIP, intrinsic pathway, TRAIL

Related Antibodies:

GABARAPL1ATG5ATG12ATG7ATG6

Rabbit polyclonalRabbit polyclonalRabbit polyclonalRabbit polyclonalRabbit polyclonal

11010-1-AP10181-2-AP11122-1-AP10088-2-AP11306-1-AP

Related Publications

A. Sengupta et al., J. Biol. Chem., 284, 41 (2009)C. Kassiotis et al., Circulation, 120, S1 (2009)

Related Antibodies:

CD40cIAP1 (BIRC2)cIAP2 (BIRC3)FASFASTNFR1TRAF1TRAF3TRAF4TRAF5TRAF6TRAF7

Rabbit polyclonalRabbit polyclonalRabbit polyclonalRabbit polyclonalmouse monoclonalRabbit polyclonalRabbit polyclonalRabbit polyclonalRabbit polyclonalRabbit polyclonalRabbit polyclonalRabbit polyclonal

12971-1-AP10022-1-AP10058-1-AP13098-1-AP60196-1-Ig21574-1-AP11543-1-AP18099-1-AP10083-2-AP12868-1-AP12809-1-AP11780-1-AP


Peters AL and Bishop GA, J Immunol. 2010;185(11):6555-62Hostager BS, Fox DK, Whitten D et al., PLoS One. 2010;5(6):e11380Akao Y, Nakagawa Y, Iio A et al., Leuk Res. 2009;33(11):1530-8.Varfolomeev E, Goncharov T, Fedorova AV et al., J Biol Chem. 2008;283(36):24295-9.

Our cIAP1 (BIRC2) antibody: aiding research on the CD40 signaling complex

1.

2.

3.

4.

1.2.

If the antibody you’re looking for is not here, please check our website.

Proteintech Group

Recent Publications

Richards JB et al.,PLoS Genet.,2009;5(12):e1000768Recent Publications

Roy R et al.,J Biol Chem.,2011 Apr 14Frohlich C et al.,Mol Cancer Res.,2011 Aug 29

Recent PublicationsLi J et al.,J Virol.,2011 Jul;85(13):6319- 33Chen X et al.,J Huazhong Univ Sci Technolog Med Sci.,2011 Apr;31(2):235- 40

Chen W et al.,Biochem Pharmacol.,2010 Jul 15;80(2):247-54Recent Publications

Iwasawa R et al.,EMBO J.,2011 Feb 2;30(3):556-68Recent Publications

Recent Publications

Yu JQ et al.,Cancer Epidemiol.,2011 Sep 19Zhang J et al.,Cancer.,2011 Jan 1;117(1):86-95


Recent PublicationsLiu H et al.,Eur J Pharmacol.,2011 Mar 11;654(3):209-16Zheng S et al.,PLoS One.,2011;6(6):e21064

Peters AL et al.,J Immunol.,2010 Dec 1;185(11):6555-62 Hostager BS et al.,PLoS One.,2010;5(6):e11380

Recent Publications

Tang F et al.,PLoS One.,2011;6(9):e24367Recent Publications

Wang B et al.,Genes Dev.,2009 Mar 15;23(6):729-39Recent Publications

Recent PublicationsLiu H et al.,Eur J Pharmacol.,2011 Mar 11;654(3):209-16Chen W et al.,Biochem Pharmacol.,2010 Jul 15;80(2):247-54

Recent PublicationsLee KJ et al.,Biochem Biophys Res Commun.,2010 Sep 3;399(4):711-5Hohberger B et al.,FEBS Lett.,2009 Feb 18;583(4):633-7

Rahman SM et al.,Cancer Res.,2011 Apr 15;71(8):3009-3017Recent Publications


Proteintech Group

Aggarwal P et al.,Cancer Cell.,2010 Oct 19;18(4):329-40Recent Publications

Porter TD et al.,Drug Metab Dispos.,2011 Mar 2Recent Publications

Weitzel DH et al.,Cell Signal.,2011 Jan;23(1):297-303Recent Publications

Recent PublicationsSong S et al.,J Pharmacol Exp Ther.,2011 Sep 13Ben Sahra I et al.,Cancer Res.,2011 May 3

Zhang J et al.,Mol Cancer.,2010;9:211Recent Publications

Recent PublicationsChopy D et al.,J Virol.,2011 Apr 27Furr SR et al.,J Neurovirol.,2008;14(6):503-13

Nakamura Y et al.,Mol Cell Biol.,2011 May 16Recent Publications

Yang M et al.,Environ Mol Mutagen.,2008 Jun;49(5):368-73Recent Publications

Recent PublicationsZhao X et al.,Neurosci Lett.,2010 Jul 26;479(2):175-9Insinna C et al.,Neural Dev.,2010 Apr 22;5(1):12

Labitzke EM et al.,Arch Biochem Biophys.,2007 Dec 1;468(1):70-81Recent Publications

Recent PublicationsKozawa E et al.,Arthritis Rheum.,2011 Oct 3


Xi L et al.,J Cell Mol Med.,2011 Jan 20Recent Publications

Griffitts J et al.,J Lipid Res.,2009 Apr;50(4):611-22Recent Publications

Cheng K et al.,J Neurosci.,2011 Aug 17;31(33):11905-13Recent Publications

Recent PublicationsShirendeb U et al.,Hum Mol Genet.,2011 Apr 1;20(7):1438-55Calkins M et al.,Hum Mol Genet.,2011 Aug 25

Recent PublicationsChen W et al.,Biochem Pharmacol.,2010 Jul 15;80(2):247-54

Recent PublicationsOkae H et al.,Dev Dyn.,2010 Apr;239(4):1089-101Haider NB et al.,Exp Eye Res.,2009 Sep;89(3):365-72

Nagpal JK et al.,Mod Pathol.,2008 Aug;21(8):979-91Recent Publications

Wang AL et al.,PLoS One.,2009;4(4):e5304Recent Publications

Li P et al.,Cell Mol Life Sci.,2010 Sep;67(18):3197-208Recent Publications

Recent PublicationsShu L et al.,AAPS J.,2011 Sep 22


Proteintech Group

A research paper featuring two Protein-tech antibodies (Lc3a - 12135-1-AP - and Atg8 - 11010-1-AP) released in July 2010 shed light on how far the reaches of the autophagic process might go – that is beyond the recycling and degradation of cellular material to the higher order functions of mammals such as balance-sensing in mice.

Autophagy is a cellular, degradative process required for cellular homeostasis and organismal viability in all eukary-otes. This process breaks down interior cell structures – such as defective organelles or internalized pathogens – that are generally too large for other degradative systems.

The process of autophagy engulfs portions of the cell by a double-membrane vesicle called an “autophagosome” – in response to a variety of internal or external instructions – and followed by its fusion with a lysosome containing all the necessary degradative machinery, namely acidic hydrolases. The former’s content and inner membrane are then de-graded by the hydrolases and lysosomal acidic environment. Essentially, autophagy is a cell janitor or caretaker, sweep-ing away any unwanted cellular components or anything that might otherwise cause the cell damage.

When regulated properly, autophagy is a process that promotes normal cellular and developmental processes, whereas its malfunction leads to an array of human diseases and contributes to aging. However, work published last year in The Journal of Clinical Investigation[1] suggests the influence of autophagy extends beyond the cellular level and may have a role in higher-order processes of organismal physiology – in other words, maintenance of cell homeostasis might not be the only balancing act in which autophagy plays a role...

“Unbalanced” miceA team lead by Carlos López-Otín at the University of Oviedo, Spain [1], investigated a novel role for autophagy in mouse sense of balance – or equilibrioception, to give it its more technical name. At the molecular level, the researchers noted that mice deficient in autophagin-1 protease (Atg4b–/–), encoded by the Atg4b gene, had increased levels of p62 protein along with an accumulation of ubiquitinylated (degradation-marked) proteins when compared to control mice. (p62 protein levels negatively correlate with autophagic flux and are a good indication of reduced autophagy.)

López-Otín and colleagues subsequently discovered that autophagy reduction in these mice occurred through defective proteolytic processing of the autophagosome component LC3; ultimately, this compromised the rate of autophagosome maturation. Yet, it was not the molecular changes that most struck the researchers about the mutant mice, it was their behavior. They not only had substantial reduction of autophagic activity, but also displayed some unusual behavioral patterns, characteristic of inner-ear disorders.

López-Otín and his fellow researchers noted that Atg4b-null mice maintained a tilted position of the head, adopted circling behaviors and had a tendency to crawl and walk

“Unbalanced” mice tip the balance on autophagy

backwards when placed outside their cages. Themice also to routinely failed both balance testing on a rota-rod tread-mill and swim tests, (all unsuccessful mice were saved from drowning in the latter case!)

An unusual discoveryInvestigating a variety of potential explanations, the Oviedo team found that the mice did not exhibit defects such as increased apoptosis or show any signs of central nervous system damage which might explain their “unbalanced” behavior. Neither did they find any gross morphological defects upon examination of the middle- and inner-ear. However, upon closer inspection of the Atg4b–/– inner-ear, they found defects in the development of the otoconia – very useful and fascinating components of the balance system in the inner ear.

Otoconia are small, organic crystals of calcium carbonate that coat the saccule and utricle of the equilibriocep-tion vestibular system. They are required for the spatial detection of gravity and linear acceleration, stimulating the cilia of the saccule and utricle epithelium by their move-ment relative to their surrounding, gelatinous supporting substrate called the cupula. The importance of otoconia in balance-sensing is apparent in people with benign paroxys-mal positional vertigo (BPPV). BPPV is a disorder in which the changing of the head’s position with respect to gravity leads to sudden vertigo; it results from the dislodging of otoconia from the saccule and utricle and their becoming trapped in other vestibular structures of the inner-ear.

What López-Otín and his colleagues found in the case of Atg4b–/– mice was that many totally lacked otoconia in the utricle and saccule, whereas others presented mildly abnormal or giant otoconia. Utricular and saccular regions from affected Atg4b–/– mice presented an accumulation of abnormal extracellular vesicle-like structures thought to be the precursors of mature otoconial crystals. This indicated

that the mice had problems secreting the necessary otoco-nial core proteins into the vestibular lumen. This prompted López-Otín and his team to look at alterations in vesicle sorting complexes and whether aberrations in autophagy might affect their workings.

Solving the puzzleThe Oviedo team was given clues on where to begin their search by previously established murine models of balance disorders, well-characterized for their underlying muta-tions. Some of these strains showed otoconial abnormali-ties due to deficiencies in components of the Bloc-1 and Ap-3 vesicle sorting complexes [2] and it was these two protein complexes that now came under scrutiny in the López-Otín lab’s studies. When the lab pharmacologically inhibited autophagy in cell lines lacking either Atg4b–/– and Atg5–/– for prolonged periods of time, they found a clear reduction in the mRNA levels of several subunits of both Bloc-1 and Ap-3. Consistent with this finding, other researchers had recently proposed a role for autophagy in melanogenesis, another process for which the activity of Ap-3 and Bloc-1 sorting complexes are essential [3].

With this work, López-Otín and his lab have not only uncovered new features of balance-sensing in higher mam-mals but also, fundamentally, they have emphasized a role for autophagy that extends beyond the individual cell. As peer researchers Andreas Till andSuresh Subramanifrom University of California San Diego, La Jolla, CA, write in their ensuing review: “The intriguing aspect of this work is that an autophagy block impairs the secretion and assembly of otoconial proteins, emphasizing a role for autophagy in functions distinct from macromolecule degradation.” [4]

Related Antibodies:

Lc3Atg8

Rabbit polyclonalRabbit polyclonal

12135-1-AP11010-1-AP


Keywords: Autophagy, Autophagosome, Atg8, LC3, mouse models, balance-sensing, equilibrioception, p62, otoconia,

G Mariño et al., J Clin Invest.2010 Jul 1120(7)2331-44JS Bonifacino, Ann N Y Acad Sci. 2004;1038:103–114.AK Ganesan et al., PLoS Genet. 2008;4(12):e1000298.A Till and S Subramani, J Clin Invest. 2010;120(7):2273–2276.

1.2.3.4.

Cleavage ofcaspase substrates

DNA

SurvivalGenes

APOPTOSIS

Degradation

DNA damage

IntrinsicPathway

Stress Signals

SURVIVAL

DNA

Deathgenes

Ca2+ rises,ER Stress

SURVIVALFACTORS

Ca2+- inducedCell Death Pathways

Extrinsic PathwayDeath Ligand

Apoptosis, derived from the Greek word for “falling off” or “dropping off” (like leaves from a tree), is defined by distinct morphological and biochemical changes. These changes are mediated by a family of cysteine aspartic acid-specific proteases (caspases), which are expressed as inactive precursors or zymogens (pro-caspases) and are proteolytically processed to an active state following an apoptotic stimulus. To date, 14

mammalian caspases have been identified and these can be roughly divided into three functional groups: apoptosis initiators (including caspase-2, -9, -8, -10), apoptosis effectors (including caspase-3, -6, -7), and cytokine maturation caspases (including caspase-1, -4, -5, -11, -12, -13, -14).

AIF

Proteintech Group

Recent PublicationsDang L et al.,Nature.,2009 Dec 10;462(7274):739-44Ogihara T et al.,J Biol Chem.,2010 Feb 19;285(8):5392-404

Recent PublicationsChen G et al.,Oncogene.,2010 Mar 11;29(10):1498-508 Wang Y et al.,Clin Cancer Res.,2007 Jul 15;13(14):4111-6

Recent PublicationsLi J et al.,Carcinogenesis.,2008 Jul;29(7):1373-9Tzouvelekis A et al.,Respir Res.,2009;10:14

Recent PublicationsBehbahani H et al.,Neurochem Int.,2010 Nov;57(6):668-75 Chandiramani N et al.,PLoS One.,2011;6(1):e14485

Recent Publications

Nin M et al.,J Dermatol Sci.,2009 Apr;54(1):17-24Recent Publications

Zheng J et al.,J Neurochem.,2011 Apr;117(1):143-53Recent Publications

Recent PublicationsLin CL et al.,Chin Med J (Engl).,2005 Jan 5;118(1):20-6


Recent PublicationsGao C et al.,Med Oncol.,2011 Sep 11

13

Recent Publications

Rodríguez-Navarro JA et al.,Hum Mol Genet.,2008 Oct 15;17(20):3128-43 Yang JY et al.,BMC Cancer.,2010;10:388

Cunha IW et al.,Transl Oncol.,2010 Feb;3(1):23-32Recent Publications

Du R et al.,J Proteome Res.,2010 Apr 5;9(4):1805-21Recent Publications

Recent Publications

Cocas LA et al.,J Neurosci.,2011 Apr 6;31(14):5313-5324 Teissier A et al.,Cereb Cortex.,2011 Jun 10

Li H et al.,Cancer Lett.,2010 Nov 28;297(2):198-206Recent Publications

Recent PublicationsOverton JD et al.,J Biol Chem.,2011 Apr 1Jiao J et al.,Biochim Biophys Acta.,2009 Oct;1792(10):1027-35

Zhang H et al.,Mol Cell Biochem.,2011 May 18Recent Publications

Wei Y et al.,J Cell Mol Med.,2010 Mar 9Yuan G et al.,Cell Signal.,2008 Jul;20(7):1284-91

Recent Publications

Recent PublicationsHaussecker D et al.,Nat Struct Mol Biol.,2008 Jul;15(7):714-21 Cao D et al.,RNA.,2009 Nov;15(11):1971- 9

Li C et al.,J Surg Oncol.,2010 Nov 23Recent Publications

Xu B et al.,Mol Cell Biochem.,2011 Apr;350(1-2):207-13Recent Publications

Recent PublicationsAlvarez-Fischer D et al.,Nat Neurosci.,2011 Sep 4Shen SM et al.,FEBS Lett.,2011 Jun 12

Zheng Z et al.,J Immunol.,2011 Aug 1Recent Publications


Proteintech Group

Albino D et al.,Cancer.,2008 Sep 15;113(6):1412-22Recent Publications

Rune A et al.,Diabetologia.,2009 Oct;52(10):2182-9Recent Publications

Yun C et al.,J Cell Biol.,2008 Nov 17;183(4):589-95Recent Publications

Recent PublicationsOsawa T et al.,Neuropathology.,2011 Feb 1 Meng Q et al.,Mol Biol Rep.,2011 Jun 17

Chen W et al.,Biochem Pharmacol.,2010 Jul 15;80(2):247-54Recent Publications

Recent Publications

Lu WG et al.,Sheng Li Xue Bao.,2007 Feb 25;59(1):51-7Sarkar J et al.,Am J Physiol Lung Cell Mol Physiol.,2010 Dec;299(6):L861-71

Li J et al.,BMC Cancer.,2010;10:354Recent Publications

Huang Y et al.,Endocr Relat Cancer.,2011;18(1):13-26Recent Publications

Lillvis JH et al.,BMC Med Genet.,2011 Jan 19;12(1):14Recent Publications

Recent PublicationsSun D et al.,Melanoma Res.,2011 Aug;21(4):335-43


Recent PublicationsKupperman E et al.,Cancer Res.,2010 Mar 1;70(5):1970-80 Soucy TA et al.,Nature.,2009 Apr 9;458(7239):732-6

Braber S et al.,Am J Physiol Lung Cell Mol Physiol.,2011 Feb;300(2):L255-65Recent Publications

Recent PublicationsSteensgaard M et al.,Acta Physiol (Oxf).,2010 Dec;200(4):347-59

Recent PublicationsHo J et al.,J Proteome Res.,2009 Feb;8(2):583-94

Recent PublicationsLucas ME et al.,J Biol Chem.,2009 May 29;284(22):14698-709 Rajandram R et al.,Nephrology (Carlton).,2009 Apr;14(2):205-12

Recent PublicationsWen Y et al.,Ann Surg Oncol.,2011 Mar 26 Hesson LB et al.,Mol Cancer.,2009;8:42

Recent PublicationsGanley IG et al.,J Biol Chem.,2009 May 1;284(18):12297-305 Wang D et al.,PLoS One.,2011;6(5):e19629

Yu N et al.,Mediators Inflamm.,2011;2011:670613Recent Publications

Zhang C et al.,Mol Cancer Ther.,2011 May 6Recent Publications

Weihofen A et al.,Biochemistry.,2009 Mar 10;48(9):2045-52Recent Publications


Proteintech Group

Recent PublicationsThiele H et al.,Hum Mutat.,2010 Nov;31(11):E1836-50Rice GI et al.,Nat Genet.,2009 Jul;41(7):829-32

Recent PublicationsBijsmans IT et al.,Mod Pathol.,2011 Mar;24(3):463-70 Rodriguez FJ et al.,J Neuropathol Exp Neurol.,2008 Dec;67(12):1194-204

Yoon HY et al.,Biol Cell.,2011 Apr 1;103(4):171-84Recent Publications

Recent PublicationsHasdemir B et al.,J Biol Chem.,2009 Oct 9;284(41):28453-66Malik R et al.,Mol Biol Cell.,2010 Jul 15;21(14):2529-41

Caron E et al.,Mol Syst Biol.,2011;7:533Recent Publications


Kim S et al.,Carcinogenesis.,2010 Apr;31(4):597-606Recent Publications

Recent PublicationsChen W et al.,Biochem Pharmacol.,2010 Jul 15;80(2):247-54Zhang J et al.,Mol Cancer.,2010;9:211

Wang P et al.,Nat Immunol.,2010 Oct;11(10):912-9Recent Publications

Recent PublicationsKido T et al.,PLoS One.,2011;6(7):e22979 Eyler CE et al.,Cell.,2011 Jul 8;146(1):53- 66

Zhu X et al.,Oral Oncol.,2011 Jun 6Recent Publications

Weinert BT et al.,Sci Signal.,2011;4(183):ra48Recent Publications

Shibata E et al.,Mol Cell Biol.,2011 May 31Recent Publications

Zhong N et al.,Biochem Biophys Res Commun.,2005 Dec 16;338(2):855-61Recent Publications

Baba Y et al.,Lab Invest.,2009 Dec;89(12):1340-7Recent Publications

Zhang J et al.,Int J Cancer.,2010 May 1;126(9):2229-39Recent Publications


Proteintech Group

Hao J et al.,Tumour Biol.,2008;29(3):195-203Recent Publications

Recent PublicationsChen N et al.,Hum Pathol.,2009 Jul;40(7):950-6 Liao Y et al.,Exp Eye Res.,2009 Jan;88(1):4-11

Ehses S et al.,J Cell Biol.,2009 Dec 28;187(7):1023-36Recent Publications

Recent PublicationsWang S et al.,Pathol Int.,2010 Mar;60(3):184-92

Fu D et al.,Mol Cell Biol.,2010 May;30(10):2449-59Recent Publications


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