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c-IAP2 monoclonal antibody (human) (16E-6-3)

ALX-803-341-C100 100 µg 353.00 USD
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Product Details

Alternative Name:HIAP-1, BIRC3, Baculoviral IAP repeat-containing protein-3, Cellular inhibitor of apoptosis-2, Human inhibitor of apoptosis protein-1, RNF49, API2
Immunogen:GST-fusion product of the CARD domain of human c-IAP2.
UniProt ID:Q13489
Species reactivity:Human
Crossreactivity:Does not cross-react with mouse c-IAP2. Does not cross-react with human or mouse c-IAP1.
Recommended Dilutions/Conditions:Western Blot (1:500-1:2,000)
Suggested dilutions/conditions may not be available for all applications.
Optimal conditions must be determined individually for each application.
Purity Detail:Protein G affinity purified.
Formulation:Liquid. 0.2µm-filtered solution in PBS. 
Handling:Avoid freeze/thaw cycles. After opening, prepare aliquots and store at -80°C.
Shipping:Blue Ice
Short Term Storage:+4°C
Long Term Storage:-80°C
Scientific Background:The inhibitor of apoptosis protein (IAP) family consists of an evolutionarily conserved group of apoptosis inhibitors containing a conserved 70 aa BIR (baculovirus inhibitor repeat) domain. Human members of the family include c-IAP1, c-IAP2, XIAP, survivin, livin and NAIP. Overexpression of IAP family members, particularly survivin and livin, in cancer cell lines and primary tumors suggests an important role for these proteins in cancer progression. In general, the IAP proteins function through direct interactions to inhibit the activity of several caspases, including caspase-3, caspase-7 and caspase-9. In addition, binding of IAP family members to the mitochondrial protein Smac blocks its interaction with caspase-9, thereby allowing the processing and activation of the caspase.
Regulatory Status:RUO - Research Use Only

Product Literature References

Biomarker profile for prediction of response to SMAC mimetic monotherapy in pediatric precursor B-cell acute lymphoblastic leukemia: J. Zinngrebe, et al.; Int. J. Cancer 146, 3219 (2020), Abstract; Full Text
Targeting Triple-Negative Breast Cancers With the Smac-mimetic Birinapant: N. Lalaoui, et al.; Cell Death Differ. 27, 2768 (2020), Abstract; Full Text
Smac mimetic induces an early wave of gene expression via NF-κB and AP-1 and a second wave via TNFR1 signaling: N. Schmidt, et al.; Cancer Lett. 421, 170 (2018), Abstract;
Combination of IAP antagonist and IFNγ activates novel caspase-10- and RIPK1-dependent cell death pathways: M.C. Tanzer, et al.; Cell Death Differ. 24, 481 (2017), Abstract; Full Text
Molecular determinants of Smac mimetic induced degradation of cIAP1 and cIAP2: M. Darding, et al.; Cell Death Differ. 18, 1376 (2011), Abstract; Full Text
TAK1 is required for survival of mouse fibroblasts treated with TRAIL, and does so by NF-kappaB dependent induction of cFLIPL: J.M. Lluis, et al.; PLoS One 5, e8620 (2010), Abstract; Full Text
Cellular IAPs inhibit a cryptic CD95-induced cell death by limiting RIP1 kinase recruitment: P. Geserick, et al.; J. Cell Biol. 187, 1037 (2009), Abstract; Full Text
TRAF2 must bind to cellular inhibitors of apoptosis for tumor necrosis factor (tnf) to efficiently activate nf-{kappa}b and to prevent tnf-induced : J.E. Vince, et al.; J. Biol. Chem. 284, 35906 (2009), Abstract;
TWEAK-FN14 signaling induces lysosomal degradation of a cIAP1-TRAF2 complex to sensitize tumor cells to TNFalpha: J.E. Vince, et al.; J. Cell. Biol. 182, 171 (2008), Abstract; Full Text
IAP antagonists target cIAP1 to induce TNFalpha-dependent apoptosis: J.E. Vince, et al.; Cell 131, 682 (2007), Abstract;
Determination of cell survival by RING-mediated regulation of inhibitor of apoptosis (IAP) protein abundance: J. Silke, et al.; PNAS 102, 16182 (2005), Abstract; Full Text

General Literature References

Destabilizing influences in apoptosis: sowing the seeds of IAP destruction: S.J. Martin; Cell 109, 793 (2002), Review, Abstract;

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