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anti-Human BIRC3 Antibodies:
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Human Monoclonal BIRC3 Primary Antibody for IP, WB - ABIN967367
Deveraux, Reed: IAP family proteins--suppressors of apoptosis. in Genes & development 1999
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Human Monoclonal BIRC3 Primary Antibody for IP, WB - ABIN967366
Goyal: Cell death inhibition: keeping caspases in check. in Cell 2001
Show all 7 Pubmed References
Human Polyclonal BIRC3 Primary Antibody for IHC (p), ELISA - ABIN545632
Jönsson, Paulie, Grandien: cIAP-2 block apoptotic events in bladder cancer cells. in Anticancer research 2003
Show all 3 Pubmed References
Human Polyclonal BIRC3 Primary Antibody for ICC, IF - ABIN4298725
Almubarak, Jones, Chaisuparat, Zhang, Meiller, Scheper: Zoledronic acid directly suppresses cell proliferation and induces apoptosis in highly tumorigenic prostate and breast cancers. in Journal of carcinogenesis 2011
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Human Polyclonal BIRC3 Primary Antibody for ICC, IF - ABIN439961
Guicciardi, Mott, Bronk, Kurita, Fingas, Gores: Cellular inhibitor of apoptosis 1 (cIAP-1) degradation by caspase 8 during TNF-related apoptosis-inducing ligand (TRAIL)-induced apoptosis. in Experimental cell research 2010
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Human Polyclonal BIRC3 Primary Antibody for IHC (p), WB - ABIN390069
Wang, Wang, Evers: Induction of cIAP-2 in human colon cancer cells through PKC delta/NF-kappa B. in The Journal of biological chemistry 2003
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Human Polyclonal BIRC3 Primary Antibody for IHC (fro), IHC (p) - ABIN252132
Jo, Park, Cha, Ahn, Kim, Kim, Koo, Jeong, Park, Dong, Lee: Cellular inhibitor of apoptosis protein 2 promotes the epithelial-mesenchymal transition in triple-negative breast cancer cells through activation of the AKT signaling pathway. in Oncotarget 2018
Human Polyclonal BIRC3 Primary Antibody for IHC, IHC (fro) - ABIN4298718
Schuster, Malinowsky, Liebmann, Berg, Wolff, Tran, Schott, Reu, Neumann, Faber, Höfler, Kirchner, Becker, Hlubek: Antibody validation by combining immunohistochemistry and protein extraction from formalin-fixed paraffin-embedded tissues. in Histopathology 2012
Human Polyclonal BIRC3 Primary Antibody for IHC (p), IHC - ABIN151193
Shen, Esnault, Schinzel, Borner, Malter: The peptidyl-prolyl isomerase Pin1 facilitates cytokine-induced survival of eosinophils by suppressing Bax activation. in Nature immunology 2009
High BIRC3 expression is associated with Oral squamous cell carcinoma.
NAIP expression is most abundant in M2 macrophages, while cIAP1 and cIAP2 show an inverse pattern of expression in polarized cells, cIAP2 is preferentially expressed in M1-macrophages and cIAP1 in M2-macrophages. IAP antagonist treatment of resting M0 macrophages preceding polarization stimulation, induced upregulation of NAIP in M2 and downregulation of cIAP1 in M1 and M2 but an induction of cIAP2 in M1 macrophages.
Results indicate that Pellino-1 contributes to lung oncogenesis through the overexpression of inhibitor of apoptosis protein 2 (cIAP2) and promotion of cell survival and chemoresistance.
We show that BIRC3 has a unique role in facilitating glioma progression from low- to high-grade
CIAP2 expression was elevated in human GBC tissues.
destabilization of TRAF2 by miR-17 reduced the ability of TRAF2 to associate with cIAP2, resulting in the downregulation of TNF-alpha-induced NF-kappaBp65, c-Jun, and STAT3 nuclear translocation and the production of IL-6, IL-8, MMP-1, and MMP-13 in human rheumatoid arthritis synovial fibroblasts.
The expression of cIAP2 mRNA was significantly higher in the groups with Helicobacter pylori(+), atrophic gastritis/intestinal metaplasia(+), and Helicobacter pylori-positive early gastric cancer than in the control, Helicobacter pylori(+), and atrophic gastritis/intestinal metaplasia(-) groups.
Polymorphisms in the BIRC3 gene are associated with a protective effect with regards to asthma susceptibility, and a reduced load of inflammatory cells.
we indicated that miR-34a can inhibit tumor invasion and metastasis in osteosarcoma, and its mechanism may be partly related to downregulating the expression of C-IAP2 and Bcl-2 protein directly or indirectly.
Study demonstrate that BIRC3 expression increases secondary to acquisition of temozolomide TMZ and irradiation resistance in glioblastoma.
High BIRC3 expression is associated with pancreatic cancer.
Network analysis identified BIRC3 as pathogenic gene in childhood asthma.
The clinical impact of small subclones harboring NOTCH1, SF3B1, or BIRC3 mutations in chronic lymphocytic leukemia patients appears to be less pronounced than that of small TP53 mutated subclones.
cIAP1 and cIAP2 mediate BCL10 ubiquitination essential for BCR-dependent NF-kB activity in the ABC subtype of DLBCL. cIAP1/2 attach K63-linked polyubiquitin chains on themselves and on BCL10, recruiting IKK and LUBAC essential for IKK activation.
Data indicate that Smac/DIABLO showed an inverse correlation with inhibitor of apoptosis proteins XIAP, cIAP-1 and cIAP-2.
cIAP2 is upregulated in regenerative epithelial cells both in ulcerative colitis and in experimental intestinal wounds. Inhibition of cIAP2 decreases wound healing in vitro possibly through inhibition of migration. [review]
LapR cells possessed increased levels of 2 of the inhibitors of apoptosis (IAPs), survivin and c-IAP-2, which are reported to block caspase activation downstream of cytosolic cytochrome C release.
API2-MALT1 induces paracaspase-mediated cleavage of the tumour suppressor protein LIMA1.
this study candidates BIRC3 as one of the potentially useful predictive marker for discriminating patients with oesophageal and oesophagogastric junction adenocarcinoma who will most likely benefit from preoperative chemoradiotherapy.
CIAP1 and cIAP2 represent novel therapeutic targets for the prevention of spontaneous preterm birth.
Shigella hijacks the glomulin-cIAP1-cIAP2-inflammasome axis to promote inflammation.
These data reveal how, upon XIAP deficiency, a TLR-TNF-TNFR2 axis drives cIAP1-TRAF2 degradation to allow TLR or TNFR1 activation of RIPK3-caspase-8 and IL-1beta. This mechanism may explain why XIAP-deficient patients can exhibit symptoms reminiscent of patients with activating inflammasome mutations.
These results reveal an additional level of regulation of the stability and the activity of E2F1 by a non-degradative K63-poly-ubiquitination and uncover a novel function for the E3-ubiquitin ligase cIAP1.
Drugs targeting XIAP and cIAP1/2 may be effective for osteosarcoma patients whose tumors express abundant RIPK1 and contain high levels of TNFalpha.
downregulation of cIAPs in PSC cholangiocytes may contribute to the development of the disease. Our results also indicate that inhibition of TRAIL signaling pathways may be beneficial in the treatment of PSC
These findings reveal a novel mechanism that endotoxin tolerance reprograms mitogen-activated protein kinase signaling by suppressing Pellino 1-mediated K63-linked ubiquitination of cIAP2, K48-linked ubiquitination, and degradation of TRAF3.
Birc3-deficient mice are resistant to azoxymethane-sodium dodecyl sulfate-induced colitis-associated colorectal cancer.
c-IAP ubiquitin protein ligase activity is required for 4-1BB signaling and CD8(+) memory T-cell survival.
Induction of cIAP2 expression upon microglia activation prevents the conversion of caspase-3 p19 subunit to p17 subunit.
we show that cIAP1 regulates TNF-induced actin cytoskeleton reorganization through a cdc42-dependentpathway
cIAP2 (Birc3)-dependent antagonism of RIPK3-mediated programmed necrosis critically protects the host from influenza infection through maintenance of pulmonary tissue homeostasis.
cIAP-2 protects cardiac fibroblasts from oxidative damage: an obligate regulatory role for ERK1/2 MAPK and NF-kappaB.
these results show that the loss of cIAP1 protects skeletal muscle from the degenerative pathology resulting from systemic loss of dystrophin.
a molecular mechanism for cIAP1's regulation in the NOD2 signaling pathway
TWEAK, cIAP1, and noncanonical NF-kappaB signaling has roles in the regulation of myoblast fusion
NFATc1 mRNA expression is negatively regulated by inhibitor of apoptosis protein 1 during osteoclastogenesis.
cIAP2 expression protects macrophages from Rip1-dependent necroptotic cell death and facilitates pathogen control.
found that, despite extensive backcrossing into a C57BL/6 background, c-IAP1(-/-) animals are also deficient in caspase 11
Our data demonstrate a novel effect of overexpressed BCL10 in the pathogenesis of high-grade MALT lymphoma by increasing expression of API2 and it then forming a protein complex with BCL10/caspase-8 leading to caspase-8 activity suppression.
This gene encodes a member of the IAP family of proteins that inhibit apoptosis by binding to tumor necrosis factor receptor-associated factors TRAF1 and TRAF2, probably by interfering with activation of ICE-like proteases. The encoded protein inhibits apoptosis induced by serum deprivation but does not affect apoptosis resulting from exposure to menadione, a potent inducer of free radicals. It contains 3 baculovirus IAP repeats and a ring finger domain. Transcript variants encoding the same isoform have been identified.
IAP homolog C
, RING finger protein 49
, TNFR2-TRAF signaling complex protein
, TNFR2-TRAF-signaling complex protein 1
, apoptosis inhibitor 2
, baculoviral IAP repeat-containing 3
, baculoviral IAP repeat-containing protein 3
, inhibitor of apoptosis protein 1
, mammalian IAP homolog C
, apoptosis inhibitor 1
, baculoviral IAP repeat-containing 2
, baculoviral IAP repeat-containing protein 3-like
, inhibitor of apoptosis protein-2