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Results indicate that Pellino-1 (show PELI1 Proteins) 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 (show TRAF2 Proteins) by miR-17 reduced the ability of TRAF2 (show TRAF2 Proteins) to associate with cIAP2, resulting in the downregulation of TNF-alpha (show TNF Proteins)-induced NF-kappaBp65, c-Jun (show JUN Proteins), and STAT3 (show STAT3 Proteins) nuclear translocation and the production of IL-6 (show IL6 Proteins), IL-8 (show IL8 Proteins), MMP-1 (show MMP1 Proteins), and MMP-13 (show MMP13 Proteins) 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 (show MLXIP Proteins)-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 (show BCL2 Proteins) 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.
These data reveal how, upon XIAP (show XIAP Proteins) deficiency, a TLR-TNF (show TNF Proteins)-TNFR2 (show TNFRSF1B Proteins) axis drives cIAP1 (show BIRC2 Proteins)-TRAF2 (show TRAF2 Proteins) degradation to allow TLR or TNFR1 (show TNFRSF1A Proteins) activation of RIPK3 (show RIPK3 Proteins)-caspase-8 (show CASP8 Proteins) and IL-1beta (show IL1B Proteins). This mechanism may explain why XIAP (show XIAP Proteins)-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 (show E2F1 Proteins) by a non-degradative K63-poly-ubiquitination and uncover a novel function for the E3-ubiquitin ligase (show MUL1 Proteins) cIAP1 (show BIRC2 Proteins).
Drugs targeting XIAP (show XIAP Proteins) and cIAP1 (show BIRC2 Proteins)/2 may be effective for osteosarcoma patients whose tumors express abundant RIPK1 (show RIPK1 Proteins) and contain high levels of TNFalpha (show TNF Proteins).
These findings reveal a novel mechanism that endotoxin tolerance reprograms mitogen-activated protein kinase (show MAPK1 Proteins) signaling by suppressing Pellino 1 (show PELI1 Proteins)-mediated K63-linked ubiquitination of cIAP2, K48-linked ubiquitination, and degradation of TRAF3 (show TRAF3 Proteins).
Birc3-deficient mice are resistant to azoxymethane-sodium dodecyl sulfate-induced colitis-associated colorectal cancer.
c-IAP (show ALPI Proteins) ubiquitin protein ligase (show UBE2K Proteins) activity is required for 4-1BB (show TNFRSF9 Proteins) signaling and CD8 (show CD8A Proteins)(+) 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 (show BIRC2 Proteins) regulates TNF (show TNF Proteins)-induced actin cytoskeleton reorganization through a cdc42 (show CDC42 Proteins)-dependentpathway
cIAP2 (Birc3)-dependent antagonism of RIPK3 (show RIPK3 Proteins)-mediated programmed necrosis critically protects the host from influenza infection through maintenance of pulmonary tissue homeostasis.
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