Affinage

BIRC3

Baculoviral IAP repeat-containing protein 3 · UniProt Q13489

Length
604 aa
Mass
68.4 kDa
Annotated
2026-06-09
100 papers in source corpus 40 papers cited in narrative 40 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 9/9 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

BIRC3 (cIAP2) is a RING-domain E3 ubiquitin ligase that governs the balance between cell survival, apoptosis, necroptosis, and inflammatory signaling by ubiquitinating key signaling substrates (PMID:18570872, PMID:18997794, PMID:31141691). Although its BIR domains bind caspases-3, -7, and -9, critical substitutions relative to XIAP render it a caspase-binding scaffold rather than a direct caspase inhibitor (PMID:16339151). Its dominant survival function is the E3 ligase-dependent K63-linked ubiquitination of RIP1/RIPK1, which it performs redundantly with cIAP1 after recruitment to the TNFR1 signalosome; this maintains canonical NF-κB survival signaling and prevents RIP1 from binding caspase-8 to trigger cell death (PMID:18570872, PMID:18697935, PMID:31141691). In parallel, cIAP2 works with TRAF2/TRAF3 to mediate constitutive proteasomal degradation of NIK, suppressing non-canonical NF-κB; loss of its RING-domain E3 activity stabilizes NIK and constitutively activates this pathway, driving B-cell hyperplasia and direct oncogenic transformation (PMID:18997794, PMID:21048983, PMID:26094954). Beyond these axes it ubiquitinates BCL10 to restrain antigen-receptor NF-κB signaling (PMID:16395405), RIP2 for NOD1/2 innate immunity (PMID:19464198), caspase-1 for inflammasome activation (PMID:22195745), and IKKε to support its kinase activity and transforming function (PMID:23453969). By limiting RIP3/RIP1 necrosome formation, cIAP2 also restrains RIPK3-dependent necroptosis, protecting against influenza A-induced epithelial death (PMID:22576661, PMID:24439895). The crystal structure of the TRAF2:cIAP2 complex shows a TRAF2 trimer engaging one cIAP2 molecule, with TRAF1 incorporation strengthening the interaction (PMID:20385093). Its abundance is set by deubiquitylases USP11 and USP35, which remove ubiquitin chains to stabilize the protein and confer therapeutic resistance (PMID:25613375, PMID:35022505). BIRC3 is transcriptionally driven by NF-κB family members (PMID:21279667, PMID:22083956), and its inactivating RING-domain mutations are associated with fludarabine-refractory chronic lymphocytic leukemia (PMID:22308293).

Mechanistic history

Synthesis pass · year-by-year structured walk · 14 steps
  1. 1997 High

    Established the first biochemical activity for cIAP2 by testing whether it directly inhibits caspases, the central question for an 'IAP' family member.

    Evidence In vitro binding/caspase activity assays, cell-free cytochrome-c extracts, and overexpression in cells

    PMID:9384571

    Open questions at the time
    • Did not assess physiological stoichiometry or endogenous relevance
    • Conflicted with later structural analysis of caspase-binding sites
  2. 2005 High

    Revised the caspase-inhibitor model by showing cIAP2 BIR domains bind but do not inhibit caspases, reframing it as a scaffold rather than an effector inhibitor.

    Evidence In vitro binding/inhibition assays with site-directed mutagenesis swapping in XIAP residues

    PMID:16339151

    Open questions at the time
    • Did not establish what the caspase-binding scaffold does in cells
    • Functional consequence of caspase binding without inhibition unresolved
  3. 2004 High

    Identified cIAP2 as an E3 ubiquitin ligase acting on RIP1, shifting the field from apoptosis inhibition to ubiquitin-mediated signaling control.

    Evidence In vitro ubiquitination assay, ectopic expression with proteasome inhibitor, and RING-domain deletion; separately, CRM1-dependent nuclear export and TRAF2 cytoplasmic retention defined

    PMID:15147886 PMID:15265700

    Open questions at the time
    • Initial study emphasized degradative RIP1 turnover rather than non-degradative chains
    • Functional role of nuclear pool of cIAP2 not defined
  4. 2006 High

    Extended E3 substrate range to BCL10 and tied loss of E3 activity to the cIAP2-MALT1 oncofusion, providing the first link between E3 inactivation and lymphomagenesis.

    Evidence In vitro ubiquitination of BCL10, NF-κB reporter, and MALT lymphoma patient sample analysis

    PMID:16395405

    Open questions at the time
    • Mechanism by which the fusion drives oncogenesis beyond BCL10 stabilization unresolved
  5. 2008 High

    Defined the dual NF-κB roles: cIAP2 maintains K63-ubiquitinated RIP1 for canonical survival signaling at TNFR1, and degrades NIK with TRAF2/3 to suppress non-canonical signaling.

    Evidence Genetic KO/RNAi, TNFR1-complex Co-IP, RIP1/IKKβ assays, NIK degradation, and Smac mimetic functional assays

    PMID:18570872 PMID:18697935 PMID:18997794

    Open questions at the time
    • Redundancy with cIAP1 complicates assigning cIAP2-specific contributions
    • Chain-type switching between K63 and K48 on shared substrates not fully resolved
  6. 2009 High

    Demonstrated cIAP2 is required for RIP2 K63-ubiquitination and NOD1/2 innate immune signaling in vivo, broadening its role to pattern-recognition immunity.

    Evidence Birc3-/- mice, RNAi, RIP2 ubiquitination assay, and in vivo MDP/colitis model; separately, NEMO-downstream genotoxic NF-κB role by RNAi epistasis

    PMID:19223549 PMID:19464198

    Open questions at the time
    • Mechanism distinguishing cIAP2 from cIAP1/XIAP in genotoxic pathway remains correlative
  7. 2010 High

    Provided atomic-resolution insight into how cIAP2 is recruited to signaling complexes via TRAF2, and how TRAF1 regulates the interaction.

    Evidence X-ray crystallography of TRAF2:cIAP2 and TRAF1:TRAF2:cIAP2 complexes with interface mutagenesis

    PMID:20385093

    Open questions at the time
    • Structures do not capture catalytically engaged RING/E2 state
    • Dynamics of recruitment to active signalosomes not visualized
  8. 2011 High

    Showed loss of cIAP2 E3 activity alone stabilizes NIK and drives non-canonical NF-κB and MALT-lymphoma-like B-cell pathology in vivo, and linked RING-domain disruption to fludarabine-refractory CLL.

    Evidence E3-inactive knock-in mice, B-cell phenotyping, and biochemical analysis of NIK/p52 in primary CLL samples; also caspase-1 inflammasome ubiquitination and translational control studies

    PMID:16813569 PMID:18195037 PMID:21048983 PMID:22195745 PMID:22308293

    Open questions at the time
    • How loss of E3 activity selectively activates non-canonical over canonical signaling not fully mechanistic
    • Cell-cycle-coupled survival role (G2/M) not integrated with signaling roles
  9. 2012 Medium

    Established cIAP2 as a brake on RIPK3-dependent necroptosis by post-transcriptionally limiting necrosome components, and expanded substrate range to viral and tumor-suppressor pathways.

    Evidence KO macrophages with Smac mimetic/RIP1 inhibitor epistasis; HBV polymerase ubiquitination assays; MDM2/p53 SUMOylation biochemistry

    PMID:21865390 PMID:22576661 PMID:23032264

    Open questions at the time
    • Mechanism of post-transcriptional RIP3 control undefined
    • MDM2/p53 link rests on RNAi in one system
  10. 2014 High

    Resolved the in vivo physiological consequence of necroptosis restraint, showing cIAP2 protects airway epithelium from RIPK3-mediated death during influenza.

    Evidence Birc3-/- mice with Ripk3 KO, RIPK1 inhibitor, and FasL/TRAIL deletion rescue

    PMID:24439895

    Open questions at the time
    • Whether protection is purely E3-dependent not directly tested
  11. 2017 Medium

    Demonstrated cIAP2 abundance is post-translationally tuned by deubiquitylases and an opposing E3, and expanded substrates to DNA-repair factor MRE11 with therapeutic relevance.

    Evidence USP11 Co-IP/ubiquitination with xenograft; ARIA-proteasome degradation; Pellino-1 K63 stabilization; cIAP2-MRE11 Co-IP and radiosensitization

    PMID:19416853 PMID:25613375 PMID:27248820 PMID:28363998

    Open questions at the time
    • Hierarchy among competing stabilizing/destabilizing regulators in vivo unknown
    • MRE11 ubiquitination chain-type and site not fully defined
  12. 2019 High

    Defined how cIAP1/2 loss together triggers caspase-8-dependent intestinal/hepatic pathology in vivo, and uncovered a 3'-UTR-dependent moonlighting role in CXCR4-mediated B-cell migration.

    Evidence Inducible cIap1/cIap2 double-KO mice with Casp8/Ripk3 epistasis and NIK inhibition; BIRC3 long-3'UTR interactome with Staufen/HuR and migration assays

    PMID:30948266 PMID:31141691

    Open questions at the time
    • 3'-UTR-dependent complex composition only partially characterized
    • Relationship between protein E3 function and mRNA-scaffolding role unclear
  13. 2022 Medium

    Reinforced deubiquitylase-mediated stabilization as a resistance mechanism, with USP35 removing K48 chains to protect cIAP2 and confer cisplatin resistance.

    Evidence Co-IP, K48-specific ubiquitination assay, and apoptosis assays in NSCLC cells

    PMID:35022505

    Open questions at the time
    • Whether USP11 and USP35 act redundantly or context-specifically not tested
  14. 2023 Medium

    Showed elevated cIAP2/NF-κB signaling enables anastatic recovery from executioner caspase activation, conferring metastatic and chemoresistant properties.

    Evidence Lineage-tracing isolation of anastatic CRC cells with cIAP2 knockdown and NF-κB inhibition

    PMID:37391410

    Open questions at the time
    • Direct substrate driving anastatic survival not identified
    • Single cancer-cell system

Open questions

Synthesis pass · forward-looking unresolved questions
  • How the diverse upstream regulators (transcriptional, translational, and stability-based) integrate to set cIAP2 levels at specific subcellular sites, and how a single RING ligase selects among K63 versus K48 chains on its many substrates in vivo, remain unresolved.
  • No unified model for chain-type selectivity across substrates
  • Functional significance of nuclear cIAP2 pool undefined
  • cIAP1/cIAP2 division of labor incompletely resolved in vivo

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140096 catalytic activity, acting on a protein 8 GO:0016874 ligase activity 7 GO:0098772 molecular function regulator activity 2 GO:0003723 RNA binding 1
Localization
GO:0005634 nucleus 1 GO:0005829 cytosol 1
Pathway
R-HSA-162582 Signal Transduction 4 R-HSA-5357801 Programmed Cell Death 4 R-HSA-1643685 Disease 3 R-HSA-168256 Immune System 3
Partners
BCL10IKBKENIKRIPK1TRAF2TRAF3USP11USP35
Complex memberships
TNFR1 signalosomeTRAF1:TRAF2:cIAP2 complexTRAF2:cIAP2 complex

Evidence

Reading pass · 40 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1997 c-IAP-2 (BIRC3) directly binds and inhibits caspases-3 and -7 in vitro (but not caspase-8, -1, or -6). The BIR domain-containing region is sufficient for caspase inhibition. Recombinant c-IAP-2 also blocked caspase activation and pro-caspase-3 processing in cell-free cytochrome-c-activated extracts and in intact cells overexpressing the protein. In vitro binding assay, in vitro caspase activity assay (Ki estimation), cell-free caspase activation system, gene transfection overexpression in intact cells The EMBO journal High 9384571
2005 Although cIAP2 BIR2 and BIR3 domains bind caspases-7 and -9, they do NOT inhibit caspase activity because of critical substitutions in the caspase-inhibitory interaction sites present in XIAP. Substituting these residues with XIAP equivalents converts cIAP2 BIR domains into tight caspase inhibitors. Thus, cIAP2 maintains a caspase-binding scaffold but lacks direct caspase inhibitory activity. In vitro binding assay, in vitro caspase inhibition assay, site-directed mutagenesis to substitute XIAP residues The Journal of biological chemistry High 16339151
2004 cIAP2 (together with cIAP1) functions as an E3 ubiquitin ligase that directly ubiquitinates RIP1 in vitro, with the RING domain required for RIP1 degradation. Expression of cIAP2 decreased steady-state RIP1 levels in a proteasome-dependent manner. In vitro ubiquitination assay, ectopic expression, proteasome inhibitor treatment, domain deletion analysis (RING mutant) FEBS letters High 15147886
2008 cIAP2 functions as an E3 ubiquitin ligase that maintains constitutive K63-linked ubiquitination of RIP1 in cancer cells, promoting association of ubiquitinated RIP1 with the pro-survival kinase TAK1. When cIAP2 is degraded (by Smac mimetic AEG40730), RIP1 becomes deubiquitinated, binds caspase-8, and triggers apoptosis. E3 ligase assay (direct ubiquitination of RIP1), co-immunoprecipitation, Smac mimetic treatment, cancer cell line functional assays Molecular cell High 18570872
2008 cIAP2 (redundantly with cIAP1) is required for RIP1 polyubiquitination and canonical NF-κB activation upon TNFα treatment. Both cIAPs are rapidly recruited to the TNFR1 signalosome upon TNFα stimulation. Combined loss of cIAP1 and cIAP2 blocks IKKβ phosphorylation and sensitizes cells to TNFα-mediated apoptosis. Combined genetic knockout and siRNA knockdown, co-immunoprecipitation with TNFR1 complex, RIP1 ubiquitination assay, IKKβ phosphorylation assay Proceedings of the National Academy of Sciences of the United States of America High 18697935
2008 cIAP2 (redundantly with cIAP1) participates in a regulatory complex with TRAF2 and TRAF3 that targets NIK for constitutive proteasome-mediated degradation, thereby suppressing non-canonical NF-κB activation. TRAF3 recruits NIK and TRAF2 recruits cIAP1/2; inhibition of both cIAPs is required for non-canonical NF-κB activation. Genetic epistasis (double cIAP1/2 inhibition required), co-immunoprecipitation, NIK degradation assay, B-cell proliferation functional assay Nature immunology High 18997794
2009 cIAP2 (encoded by Birc3) is required as an E3 ubiquitin ligase for K63-linked ubiquitination of RIP2 and for NOD1/NOD2 innate immune signaling. Birc3-/- macrophages and colonocytes show severely attenuated cytokine/chemokine production in response to NOD agonists; in vivo, Birc3-/- mice fail to be protected by MDP (NOD2 agonist) from experimental colitis. Genetic knockout (Birc3-/- mice), RNAi knockdown, RIP2 ubiquitination assay, in vivo colitis model Immunity High 19464198
2010 Crystal structures of the TRAF2:cIAP2 binary complex and the TRAF1:TRAF2:cIAP2 ternary complex were solved. A TRAF2 trimer interacts with one cIAP2 molecule; two chains of the trimer contact cIAP2. Key interface residues were confirmed by mutagenesis. TRAF1:(TRAF2)2 heterotrimers bind cIAP2 more strongly than TRAF2 homotrimers, revealing a regulatory mechanism whereby TRAF1 upregulation modulates TRAF2-cIAP2 interaction. X-ray crystallography, mutagenesis of interface residues, solution binding assays Molecular cell High 20385093
2011 cIAP2 (with cIAP1 and TRAF2) directly interacts with caspase-1-containing inflammasome complexes and mediates K63-linked (non-degradative) polyubiquitination of caspase-1, which is required for efficient caspase-1 activation. Birc3-/- mice have impaired caspase-1 activation after inflammasome stimulation and are resistant to peritonitis. Co-immunoprecipitation, K63-linked ubiquitination assay of caspase-1, genetic knockout mice, in vivo peritonitis model Immunity High 22195745
2006 cIAP2 is an E3 ubiquitin ligase for BCL10 and targets it for proteasomal degradation, thereby inhibiting antigen receptor-mediated NF-κB activation and cytokine production. The cIAP2-MALT1 fusion oncoprotein (found in MALT lymphomas) lacks E3 activity, and BCL10 is stabilized in MALT lymphomas harboring this fusion. E3 ubiquitin ligase assay (in vitro ubiquitination of BCL10), co-immunoprecipitation, BCL10 degradation assay, NF-κB reporter assay, MALT lymphoma patient sample analysis The Journal of clinical investigation High 16395405
2009 cIAP2 regulates an event downstream of NEMO ubiquitination in genotoxic stress-induced NF-κB activation, distinct from and non-redundant with the roles of XIAP (upstream TAK1 activation) and cIAP1 (NEMO ubiquitination). This places cIAP2 as a component of the genotoxic NF-κB pathway downstream of NEMO. siRNA knockdown of individual IAPs, NF-κB luciferase reporter, epistasis analysis with NEMO ubiquitination assays Cancer research Medium 19223549
2011 Loss of cIAP2 E3 ubiquitin ligase activity (via RING domain inactivation) is sufficient to stabilize NIK and activate non-canonical NF-κB signaling in vivo. Mice expressing E3-inactive cIAP2 accumulated abnormal B cells with elevated non-canonical NF-κB, gut-associated lymphoid hyperplasia, and other features resembling MALT lymphoma. Canonical NF-κB activation by cIAP2-MALT1 fusion depended on MALT1 paracaspase activity, while non-canonical activation required only loss of cIAP2 E3 activity. Knock-in mouse expressing E3-inactive cIAP2 mutant, B-cell phenotyping, NF-κB pathway activation assays, MALT1 paracaspase activity mutation PLoS biology High 21048983
2011 Smac mimetic-induced degradation of cIAP2 requires TRAF2 binding and depends on cIAP1 presence; degradation of cIAP2 also requires RING finger dimerization and E2 binding. Unlike cIAP1, cIAP2 degradation is not autonomous. The cIAP2-MALT1 oncofusion (lacking the RING) is resistant to Smac mimetic-induced degradation. Smac mimetic treatment, co-immunoprecipitation, RING domain mutants, cIAP1/2 double-knockout cell lines Cell death and differentiation Medium 21331077
2013 A cIAP1/cIAP2/TRAF2 E3 ubiquitin ligase complex binds IKKε and mediates K63-linked polyubiquitination at lysine 30 and 401. This ubiquitination is required for IKKε kinase activity, IKKε-mediated NF-κB activation, and IKKε-induced malignant transformation in breast cancer cells. Co-immunoprecipitation, in vitro K63-ubiquitination assay, site-directed mutagenesis of ubiquitination sites, kinase activity assay, transformation assay Cell reports High 23453969
2004 cIAP2 is a nuclear shuttling protein whose subcellular localization is regulated by CRM1-dependent nuclear export. TRAF2 binding retains cIAP2 in the cytoplasm, and TNFα treatment reduces this TRAF2-mediated cytoplasmic retention, potentially allowing nuclear translocation. Leptomycin B treatment, epitope-tagged protein localization, NES mutagenesis, TRAF2 co-expression experiments Experimental cell research Medium 15265700
2008 cIAP2 mRNA is translated exclusively through a stress-modulated ribosome shunting mechanism that bypasses 62 upstream AUGs in the 2.78-kb 5' UTR. A conserved RNA folding domain (1,470–1,877 nt upstream) modulates shunting efficiency. Ribosome shunting efficiency is altered by cellular stress. In vitro translation assay, transfection of RNA reporters, selective mutation of shunt-donor sequences, comparison with internal ribosome entry site controls Molecular and cellular biology High 18195037
2010 Tristetraprolin (TTP) directly binds the 2nd AU-rich element (ARE) in the 3' UTR of cIAP2 mRNA and destabilizes cIAP2 mRNA by recruiting mRNA-decapping enzyme Dcp2 and 5'-3' exonuclease Xrn1, requiring flanking nucleotides beyond the core ARE sequence. RNA EMSA, mRNA stability assay (luciferase reporter), co-immunoprecipitation of TTP/Dcp2/Xrn1, mutagenesis of AREs Biochemical and biophysical research communications Medium 20691152
2011 In glioma cells, NF-κB p65 directly transactivates cIAP2, as shown by ChIP at the BIRC3 promoter. p65-driven cIAP2 expression is required to maintain RIP1 polyubiquitination and thereby confer resistance to TNFα-mediated cell death. shRNA knockdown of p65, RT-PCR, chromatin immunoprecipitation (ChIP), RIP1 ubiquitination assay, TNFα cytotoxicity assay Journal of neuro-oncology Medium 21279667
2011 CBP histone acetyltransferase mediates NF-κB-dependent histone acetylation at an estrogen response element (ERE) in the BIRC3 promoter, enabling estrogen receptor (ER) recruitment to this ERE. NF-κB activation (acting through two response elements) is required for ER recruitment; CBP promotes both histone acetylation and ER binding at the BIRC3 promoter, leading to synergistic BIRC3 upregulation. ChIP, promoter deletion analysis, siRNA knockdown, luciferase reporter assay Molecular and cellular biology Medium 22083956
2011 In HTLV-1-transformed lymphocytes, the viral oncoprotein Tax stimulates BIRC3 (HIAP-1/cIAP2) promoter activity ~60-fold primarily through NF-κB activation. RNAi-mediated suppression of cIAP2 in these cells causes dramatic reduction of cell growth, strong induction of apoptosis, and increased caspase-3/7 activity, establishing that Tax-mediated cIAP2 overexpression is required for survival of HTLV-1-transformed lymphocytes. Promoter-reporter transfection, RNAi via lentiviral transduction, apoptosis and caspase activity assays Blood Medium 16467195
2011 cIAP2 inhibits the complete autocatalytic processing of caspase-3 from its p19 intermediate form to the fully mature p17 subunit during microglia activation, preventing full caspase-3 activation. This restrains caspase-3 activity and subcellular localization, allowing pro-inflammatory microglia activation rather than cell death. SMAC mimetic or cIAP2 siRNA reverses this effect. siRNA knockdown, SMAC mimetic (BV6), Western blot for caspase-3 subunits, immunofluorescence localization, LPS-mediated activation assay Cell death & disease Medium 25501826
2012 cIAP2 (together with cIAP1) limits RIP3 (and to a lesser extent RIP1) expression via post-transcriptional mechanisms, thereby inhibiting formation of the RIP1-RIP3 necroptotic complex (necrosome) in macrophages. Loss of cIAP function (via Smac mimetic or specific knockout) results in elevated macrophage necroptosis dependent on RIP1 kinase signaling and RIP3 expression. Smac mimetic treatment, specific cIAP knockout macrophages, RIP3 knockdown, RIP1 kinase inhibitor, protein level analysis Cell death and differentiation Medium 22576661
2014 cIAP2 deficiency in mice results in increased susceptibility to influenza A-induced mortality due to RIPK3-mediated programmed necrosis (necroptosis) of airway epithelial cells, not due to impaired antiviral immunity. Genetic deletion of Ripk3 or pharmacological inhibition of RIPK1, or deletion of death receptor agonists (FasL or TRAIL) from hematopoietic cells, rescued cIAP2-deficient mice from influenza lethality. Genetic knockout (Birc3-/- mice), Ripk3-/- and Ripk1 inhibitor epistasis, histopathology, viral replication assay, hematopoietic cell transfer Cell host & microbe High 24439895
2015 USP11 is a deubiquitylase that directly stabilizes cIAP2 protein by removing ubiquitin chains, preventing Smac mimetic-induced cIAP2 degradation. High USP11 expression correlates with cIAP2 stability and resistance to Smac mimetic-induced apoptosis. TNFα/JNK pathway induces USP11 expression to maintain cIAP2 stability as an alternative survival pathway. Co-immunoprecipitation, ubiquitination assay, USP11 overexpression/knockdown, apoptosis assay, xenograft model Cell death and differentiation Medium 25613375
2011 In BIRC3-disrupted CLL cells (via inactivating mutations or gene deletions removing the RING domain), constitutive non-canonical NF-κB signaling is activated, consistent with loss of cIAP2 E3 ligase-mediated NIK degradation. BIRC3 disruption associates specifically with fludarabine-refractory CLL. Biochemical analysis of non-canonical NF-κB activation (NIK stabilization, p52 processing) in primary CLL samples with BIRC3 mutations/deletions Blood Medium 22308293
2012 cIAP2 functions as an E3 ubiquitin ligase that promotes polyubiquitination and proteasome-mediated degradation of hepatitis B virus (HBV) polymerase. cIAP2 binds HBV polymerase, promotes its K48-linked ubiquitination, reduces encapsidation of HBV pregenomic RNA, and thereby inhibits HBV replication. An E3 ligase-deficient cIAP2 mutant loses this antiviral activity. Overexpression/knockdown of cIAP2, co-immunoprecipitation of cIAP2-polymerase, ubiquitination assay, proteasome inhibitor, HBV replication intermediates assay Journal of virology Medium 21865390
2015 NPD1 (neuroprotectin D1) induces nuclear translocation of cREL, which in turn mediates BIRC3 transcription. cREL-driven BIRC3 expression is required for NPD1-induced neural cell survival against oxidative stress; BIRC3 silencing prevents NPD1 survival induction. In vivo, brain NPD1 biosynthesis and neuronal BIRC3 abundance are increased by DHA after ischemic stroke. cREL nuclear translocation assay, BIRC3 promoter-reporter, siRNA knockdown of BIRC3, retinal pigment epithelial cell oxidative stress assay, in vivo stroke model with DHA treatment Cell death and differentiation Medium 25633199
2009 An ARIA (apoptosis regulator through modulating IAP expression) protein promotes proteasomal degradation of cIAP2 in endothelial cells without affecting cIAP2 mRNA. ARIA interacts with 20S proteasome subunit alpha-7. ARIA knockdown increases cIAP2 protein and reduces endothelial apoptosis; simultaneous knockdown of both cIAP1 and cIAP2 abolishes the ARIA-knockdown anti-apoptotic effect. siRNA knockdown, protein stability assay, yeast two-hybrid (ARIA-proteasome interaction), overexpression, co-immunoprecipitation, in vivo angiogenesis models Proceedings of the National Academy of Sciences of the United States of America Medium 19416853
2019 The long 3' UTR of BIRC3 mRNA (upregulated in leukemia) is required for CXCR4-mediated B cell migration. The long 3' UTR enables formation of additional protein complexes not present when BIRC3 is encoded from short 3' UTR mRNA, including interactors regulating CXCR4 trafficking. RNA-binding proteins Staufen and HuR cooperatively bind the long 3' UTR to mediate this 3'-UTR-dependent complex formation. Mass spectrometry interactome of BIRC3 from long vs. short 3' UTR mRNA, CXCR4 trafficking assay, B cell migration assay, Staufen/HuR RIP assay Molecular cell Medium 30948266
2006 Cell cycle-dependent expression of cIAP2 peaks at G2/M phase, mediated by a bipartite CDE/CHR element in the cIAP2 promoter. This G2/M-specific cIAP2 expression is enhanced by NF-κB but occurs independently of NF-κB. Selective downregulation of cIAP2 in nocodazole-arrested cells increases susceptibility to apoptosis, establishing a survival function specific to mitotic arrest. Cell cycle synchronization, promoter deletion/mutagenesis (CDE/CHR elements), siRNA knockdown, apoptosis assay in mitotically arrested cells The Biochemical journal Medium 16813569
2017 cIAP2 functions as an E3 ligase for MRE11 in bladder cancer cells following HDAC inhibition. cIAP2 is upregulated in response to HDAC inhibition, binds MRE11, promotes altered MRE11 ubiquitination and downregulation, and mediates radiosensitization. Overexpression of cIAP2 alone recapitulates the effects of HDAC inhibition on MRE11 levels. Co-immunoprecipitation (cIAP2-MRE11), ubiquitination assay, cIAP2 overexpression, radiosensitization assay, HDAC inhibitor treatment Cancer research Medium 28363998
2016 BIRC3 expression is upregulated in GBM in response to irradiation and temozolomide treatment through STAT3 and PI3K signaling pathways. BIRC3 upregulation promotes apoptosis evasion and therapeutic resistance; selective inhibition of BIRC3 reverses resistance. BIRC3 expression analysis after RT/TMZ, pathway inhibitor treatment (STAT3/PI3K), functional apoptosis assay in GBM cell lines and in vivo xenografts Scientific reports Medium 26888114
2019 cIAP2 upregulation in CRC cells following Fusobacterium nucleatum infection is mediated via the TLR4/NF-κB pathway, and this cIAP2 upregulation confers resistance to 5-fluorouracil both in vitro and in vivo. Whole genome microarray, siRNA knockdown of BIRC3, in vitro and in vivo 5-FU sensitivity assay, NF-κB pathway inhibition Journal of experimental & clinical cancer research Medium 30630498
2019 cIAP2 ubiquitinates RIPK1 to maintain NF-κB signaling and cell survival. Combined in vivo deletion of cIap2 from cIap1-deficient adult mice causes rapid inflammation and aberrant caspase-8-dependent cell death in intestine and liver; Casp8 + Ripk3 double deletion prevents this cell death and partially reduces inflammation. Residual inflammation in cIAP1/2-deficient mice is reduced by NIK inhibition. Conditional double-KO mouse (inducible cIap2 deletion in cIap1-KO background), Casp8/Ripk3/Mlkl genetic deletion epistasis, NIK inhibitor, histopathology, cleaved caspase immunoblot Cell reports High 31141691
2022 USP35 is a deubiquitylase that directly interacts with and stabilizes BIRC3 by removing K48-linked polyubiquitin chains, preventing proteasomal degradation. USP35 overexpression increases BIRC3 abundance and confers resistance to cisplatin-induced apoptosis in NSCLC cells; USP35 knockdown reduces BIRC3 and sensitizes cells to cisplatin. Co-immunoprecipitation, ubiquitination assay (K48-specific), USP35 overexpression/knockdown, BIRC3 protein stability assay, apoptosis assay Laboratory investigation Medium 35022505
2016 Pellino-1 E3 ubiquitin ligase directly interacts with cIAP2 and stabilizes it through Lys63-linked polyubiquitination, conferring chemoresistance to cisplatin and paclitaxel in lung cancer cells. Pellino-1-mediated chemoresistance is dependent on cIAP2 induction. Co-immunoprecipitation, K63-ubiquitination assay, Pellino-1 overexpression/knockdown, chemosensitivity assay, epistasis with cIAP2 knockdown Oncotarget Medium 27248820
2012 cIAP2 knockdown in mammary epithelial cells activates MDM2 through increased SUMOylation and IKKα/β-dependent phosphorylation, causing p53 degradation. cIAP2 prevents IKKα/β-mediated MDM2 activation; concomitant IKKα/β inhibition rescues p53 levels after cIAP2 knockdown. cIAP2 knockdown disrupts the PIAS1-IKKα interaction required to prevent MDM2 SUMOylation. siRNA knockdown, MDM2 SUMOylation assay, IKKα/β inhibition, immunoprecipitation of PIAS1-IKKα complex, p53 level rescue by Nutlin-3a Cell cycle Medium 23032264
2015 BIRC3 mutations that remove the RING domain (abolishing E3 ubiquitin ligase activity) confer direct oncogenic/transforming potential in a wide range of epithelial tumor cell lines. This transforming function is largely independent of canonical NF-κB activation. NIK is an important but not exclusive mediator of BIRC3-mutant-driven carcinogenesis, acting through pathways other than NF-κB. Transformation assay (focus formation, anchorage-independent growth), RING domain mutants, NF-κB reporter, NIK knockdown epistasis Cancer science Medium 26094954
2020 H. pylori CagA protein induces resistance to caspase-3-mediated apoptosis in gastric epithelial cells via Brd4-dependent synthesis of a BIRC3 enhancer RNA (eRNA), which drives BIRC3 mRNA and cIAP2 protein upregulation. Depletion of BIRC3 eRNA or inhibition of Brd4 reverses H. pylori-induced cIAP2 induction and apoptosis resistance. CagA-deficient H. pylori mutant fails to activate BIRC3 eRNA synthesis. siRNA knockdown of BIRC3 eRNA and BIRC3, Brd4 inhibitor, CagA-deficient bacterial mutant, caspase-3 activation assay, ChIP for Brd4 at BIRC3 enhancer Cell death & disease Medium 32820150
2023 During anastasis (recovery from executioner caspase activation), colorectal cancer cells upregulate cIAP2 and activate NF-κB. This elevated cIAP2/NF-κB signaling persists in anastatic cells and is required both for initial survival of caspase activation and for subsequent enhanced migration, metastasis, and chemoresistance. Lineage-tracing system to isolate anastatic cells, cIAP2 knockdown, NF-κB inhibition, caspase activation reporter, migration and chemoresistance assays Cell death & disease Medium 37391410

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1997 The c-IAP-1 and c-IAP-2 proteins are direct inhibitors of specific caspases. The EMBO journal 1060 9384571
2008 cIAP1 and cIAP2 facilitate cancer cell survival by functioning as E3 ligases that promote RIP1 ubiquitination. Molecular cell 933 18570872
2008 Noncanonical NF-kappaB activation requires coordinated assembly of a regulatory complex of the adaptors cIAP1, cIAP2, TRAF2 and TRAF3 and the kinase NIK. Nature immunology 524 18997794
2008 Both cIAP1 and cIAP2 regulate TNFalpha-mediated NF-kappaB activation. Proceedings of the National Academy of Sciences of the United States of America 453 18697935
2005 The human anti-apoptotic proteins cIAP1 and cIAP2 bind but do not inhibit caspases. The Journal of biological chemistry 301 16339151
2009 Cellular inhibitors of apoptosis cIAP1 and cIAP2 are required for innate immunity signaling by the pattern recognition receptors NOD1 and NOD2. Immunity 287 19464198
2016 Clinical impact of clonal and subclonal TP53, SF3B1, BIRC3, NOTCH1, and ATM mutations in chronic lymphocytic leukemia. Blood 285 26837699
2019 Fusobacterium nucleatum promotes chemoresistance to 5-fluorouracil by upregulation of BIRC3 expression in colorectal cancer. Journal of experimental & clinical cancer research : CR 268 30630498
2012 Disruption of BIRC3 associates with fludarabine chemorefractoriness in TP53 wild-type chronic lymphocytic leukemia. Blood 235 22308293
2007 Reduction of TRAIL-induced Mcl-1 and cIAP2 by c-Myc or sorafenib sensitizes resistant human cancer cells to TRAIL-induced death. Cancer cell 229 17613437
2010 Crystal structures of the TRAF2: cIAP2 and the TRAF1: TRAF2: cIAP2 complexes: affinity, specificity, and regulation. Molecular cell 174 20385093
2021 BIRC3 and BIRC5: multi-faceted inhibitors in cancer. Cell & bioscience 158 33413657
2011 Alteration of BIRC3 and multiple other NF-κB pathway genes in splenic marginal zone lymphoma. Blood 151 21881048
2011 Cellular inhibitors of apoptosis proteins cIAP1 and cIAP2 are required for efficient caspase-1 activation by the inflammasome. Immunity 143 22195745
2014 Cellular inhibitor of apoptosis protein cIAP2 protects against pulmonary tissue necrosis during influenza virus infection to promote host survival. Cell host & microbe 141 24439895
2003 A comprehensive search for DNA amplification in lung cancer identifies inhibitors of apoptosis cIAP1 and cIAP2 as candidate oncogenes. Human molecular genetics 133 12651874
2012 cIAP1 and cIAP2 limit macrophage necroptosis by inhibiting Rip1 and Rip3 activation. Cell death and differentiation 130 22576661
2002 Cytokine regulation of pro- and anti-apoptotic genes in rat hepatocytes: NF-kappaB-regulated inhibitor of apoptosis protein 2 (cIAP2) prevents apoptosis. Journal of hepatology 130 12044523
2004 Receptor interacting protein is ubiquitinated by cellular inhibitor of apoptosis proteins (c-IAP1 and c-IAP2) in vitro. FEBS letters 117 15147886
2017 CircDOCK1 suppresses cell apoptosis via inhibition of miR‑196a‑5p by targeting BIRC3 in OSCC. Oncology reports 114 29286141
2012 A novel small molecule FL118 that selectively inhibits survivin, Mcl-1, XIAP and cIAP2 in a p53-independent manner, shows superior antitumor activity. PloS one 108 23029106
2003 TL1A-induced NF-kappaB activation and c-IAP2 production prevent DR3-mediated apoptosis in TF-1 cells. The Journal of biological chemistry 105 12882979
2002 Expression of the inhibitor of apoptosis (IAP) family members in human neutrophils: up-regulation of cIAP2 by granulocyte colony-stimulating factor and overexpression of cIAP2 in chronic neutrophilic leukemia. Blood 100 12393423
2003 Induction of cIAP-2 in human colon cancer cells through PKC delta/NF-kappa B. The Journal of biological chemistry 93 14527959
2011 Deletion of cIAP1 and cIAP2 in murine B lymphocytes constitutively activates cell survival pathways and inactivates the germinal center response. Blood 91 21300983
2011 Molecular determinants of Smac mimetic induced degradation of cIAP1 and cIAP2. Cell death and differentiation 89 21331077
2006 cIAP2 is a ubiquitin protein ligase for BCL10 and is dysregulated in mucosa-associated lymphoid tissue lymphomas. The Journal of clinical investigation 89 16395405
2009 cIAP1, cIAP2, and XIAP act cooperatively via nonredundant pathways to regulate genotoxic stress-induced nuclear factor-kappaB activation. Cancer research 88 19223549
2009 MMP13, Birc2 (cIAP1), and Birc3 (cIAP2), amplified on chromosome 9, collaborate with p53 deficiency in mouse osteosarcoma progression. Cancer research 84 19276372
2019 LncRNA HCP5 promotes triple negative breast cancer progression as a ceRNA to regulate BIRC3 by sponging miR-219a-5p. Cancer medicine 78 31215169
2020 Biological and clinical implications of BIRC3 mutations in chronic lymphocytic leukemia. Haematologica 76 31371416
2016 BIRC3 is a novel driver of therapeutic resistance in Glioblastoma. Scientific reports 75 26888114
2014 ATM mutation rather than BIRC3 deletion and/or mutation predicts reduced survival in 11q-deleted chronic lymphocytic leukemia: data from the UK LRF CLL4 trial. Haematologica 66 24584352
2010 cIAP2 upregulated by E6 oncoprotein via epidermal growth factor receptor/phosphatidylinositol 3-kinase/AKT pathway confers resistance to cisplatin in human papillomavirus 16/18-infected lung cancer. Clinical cancer research : an official journal of the American Association for Cancer Research 65 20959404
2016 MicroRNA-17 Suppresses TNF-α Signaling by Interfering with TRAF2 and cIAP2 Association in Rheumatoid Arthritis Synovial Fibroblasts. Journal of immunology (Baltimore, Md. : 1950) 64 27534557
2014 Regulation of caspase-3 processing by cIAP2 controls the switch between pro-inflammatory activation and cell death in microglia. Cell death & disease 64 25501826
2015 USP11-dependent selective cIAP2 deubiquitylation and stabilization determine sensitivity to Smac mimetics. Cell death and differentiation 63 25613375
2013 IKKε-mediated tumorigenesis requires K63-linked polyubiquitination by a cIAP1/cIAP2/TRAF2 E3 ubiquitin ligase complex. Cell reports 62 23453969
2017 IL-1β induces up-regulation of BIRC3, a gene involved in chemoresistance to doxorubicin in breast cancer cells. Cancer letters 61 28093282
2015 Frequencies of SF3B1, NOTCH1, MYD88, BIRC3 and IGHV mutations and TP53 disruptions in Chinese with chronic lymphocytic leukemia: disparities with Europeans. Oncotarget 57 25605254
2020 Multiplex immunohistochemistry/immunofluorescence (mIHC/IF) for PD-L1 testing in triple-negative breast cancer: a translational assay compared with conventional IHC. Journal of clinical pathology 56 31969377
2019 Ubiquitin Ligases cIAP1 and cIAP2 Limit Cell Death to Prevent Inflammation. Cell reports 56 31141691
2009 cIAP2 as a therapeutic target in colorectal cancer and other malignancies. Expert opinion on therapeutic targets 56 19793002
2016 LCL161 increases paclitaxel-induced apoptosis by degrading cIAP1 and cIAP2 in NSCLC. Journal of experimental & clinical cancer research : CR 55 27737687
2005 Glucocorticoids inhibit cell death in ovarian cancer and up-regulate caspase inhibitor cIAP2. Clinical cancer research : an official journal of the American Association for Cancer Research 52 16144937
2009 Down-regulation of cIAP2 enhances 5-FU sensitivity through the apoptotic pathway in human colon cancer cells. Cancer science 50 19302291
2005 ras Oncogene triggers up-regulation of cIAP2 and XIAP in intestinal epithelial cells: epidermal growth factor receptor-dependent and -independent mechanisms of ras-induced transformation. The Journal of biological chemistry 50 16115895
2006 Requirement of the human T-cell leukemia virus (HTLV-1) tax-stimulated HIAP-1 gene for the survival of transformed lymphocytes. Blood 48 16467195
2020 Clinical significance of TP53, BIRC3, ATM and MAPK-ERK genes in chronic lymphocytic leukaemia: data from the randomised UK LRF CLL4 trial. Leukemia 45 32015491
2014 NOTCH1, SF3B1, BIRC3 and TP53 mutations in patients with chronic lymphocytic leukemia undergoing first-line treatment: correlation with biological parameters and response to treatment. Leukemia & lymphoma 45 24597984
2010 Non-canonical NF-κB activation and abnormal B cell accumulation in mice expressing ubiquitin protein ligase-inactive c-IAP2. PLoS biology 44 21048983
2019 Gain of Additional BIRC3 Protein Functions through 3'-UTR-Mediated Protein Complex Formation. Molecular cell 42 30948266
2020 SAHA and EGCG Promote Apoptosis in Triple-negative Breast Cancer Cells, Possibly Through the Modulation of cIAP2. Anticancer research 41 31892549
2000 Tumor necrosis factor-alpha-induced lung cell expression of antiapoptotic genes TRAF1 and cIAP2. American journal of respiratory cell and molecular biology 41 10657935
2021 Single-cell transcriptomic analysis of mIHC images via antigen mapping. Science advances 40 33674303
2019 Cul4 E3 ubiquitin ligase regulates ovarian cancer drug resistance by targeting the antiapoptotic protein BIRC3. Cell death & disease 40 30718461
2015 NPD1-mediated stereoselective regulation of BIRC3 expression through cREL is decisive for neural cell survival. Cell death and differentiation 40 25633199
2015 IPS-1 differentially induces TRAIL, BCL2, BIRC3 and PRKCE in type I interferons-dependent and -independent anticancer activity. Cell death & disease 40 25950488
2011 An NF-κB p65-cIAP2 link is necessary for mediating resistance to TNF-α induced cell death in gliomas. Journal of neuro-oncology 40 21279667
2012 Gene network revealed involvements of Birc2, Birc3 and Tnfrsf1a in anti-apoptosis of injured peripheral nerves. PloS one 38 23028454
2011 CBP mediates NF-κB-dependent histone acetylation and estrogen receptor recruitment to an estrogen response element in the BIRC3 promoter. Molecular and cellular biology 38 22083956
2009 Arsenic trioxide induces apoptosis in NB-4, an acute promyelocytic leukemia cell line, through up-regulation of p73 via suppression of nuclear factor kappa B-mediated inhibition of p73 transcription and prevention of NF-kappaB-mediated induction of XIAP, cIAP2, BCL-XL and survivin. Medical oncology (Northwood, London, England) 38 19763917
2017 TNFR2/BIRC3-TRAF1 signaling pathway as a novel NK cell immune checkpoint in cancer. Oncoimmunology 37 30524877
2018 BIRC3 Expression Predicts CLL Progression and Defines Treatment Sensitivity via Enhanced NF-κB Nuclear Translocation. Clinical cancer research : an official journal of the American Association for Cancer Research 36 30487125
2017 cIAP2 promotes gallbladder cancer invasion and lymphangiogenesis by activating the NF-κB pathway. Cancer science 36 28295868
2014 Antitumor activity of FL118, a survivin, Mcl-1, XIAP, and cIAP2 selective inhibitor, is highly dependent on its primary structure and steric configuration. Molecular pharmaceutics 36 24329001
2010 Rb inactivation accelerates neoplastic growth and substitutes for recurrent amplification of cIAP1, cIAP2 and Yap1 in sporadic mammary carcinoma associated with p53 deficiency. Oncogene 36 20676140
2018 A novel SMAC mimetic APG-1387 exhibits dual antitumor effect on HBV-positive hepatocellular carcinoma with high expression of cIAP2 by inducing apoptosis and enhancing innate anti-tumor immunity. Biochemical pharmacology 35 29679556
2004 Nuclear shuttling and TRAF2-mediated retention in the cytoplasm regulate the subcellular localization of cIAP1 and cIAP2. Experimental cell research 35 15265700
2018 Inhibitor of apoptosis proteins, NAIP, cIAP1 and cIAP2 expression during macrophage differentiation and M1/M2 polarization. PloS one 34 29518103
2011 Progesterone receptor-B induction of BIRC3 protects endometrial cancer cells from AP1-59-mediated apoptosis. Hormones & cancer 34 21760855
2008 Translation of cIAP2 mRNA is mediated exclusively by a stress-modulated ribosome shunt. Molecular and cellular biology 34 18195037
2022 Ubiquitin-specific protease 35 (USP35) mediates cisplatin-induced apoptosis by stabilizing BIRC3 in non-small cell lung cancer. Laboratory investigation; a journal of technical methods and pathology 33 35022505
2021 Targeting c-IAP1, c-IAP2, and Bcl-2 Eliminates Senescent Glioblastoma Cells Following Temozolomide Treatment. Cancers 33 34298797
2017 E3 Ligase cIAP2 Mediates Downregulation of MRE11 and Radiosensitization in Response to HDAC Inhibition in Bladder Cancer. Cancer research 33 28363998
2015 TAK1-regulated expression of BIRC3 predicts resistance to preoperative chemoradiotherapy in oesophageal adenocarcinoma patients. British journal of cancer 31 26291056
2016 Pellino-1 confers chemoresistance in lung cancer cells by upregulating cIAP2 through Lys63-mediated polyubiquitination. Oncotarget 30 27248820
2015 Oncogenic activity of BIRC2 and BIRC3 mutants independent of nuclear factor-κB-activating potential. Cancer science 29 26094954
2009 Identification of ARIA regulating endothelial apoptosis and angiogenesis by modulating proteasomal degradation of cIAP-1 and cIAP-2. Proceedings of the National Academy of Sciences of the United States of America 28 19416853
2016 NOR-1/NR4A3 regulates the cellular inhibitor of apoptosis 2 (cIAP2) in vascular cells: role in the survival response to hypoxic stress. Scientific reports 27 27654514
2009 Malt1 and cIAP2-Malt1 as effectors of NF-kappaB activation: kissing cousins or distant relatives? Cellular signalling 27 19772915
2021 Regulation of Anti-Apoptotic SOD2 and BIRC3 in Periodontal Cells and Tissues. International journal of molecular sciences 26 33435582
2013 UVB-induced anti-survival and pro-apoptotic effects on HaCaT human keratinocytes via caspase- and PKC-dependent downregulation of PKB, HIAP-1, Mcl-1, XIAP and ER stress. International journal of molecular medicine 26 24356997
2024 E3 ubiquitin ligase gene BIRC3 modulates TNF-induced cell death pathways and promotes aberrant proliferation in rheumatoid arthritis fibroblast-like synoviocytes. Frontiers in immunology 25 39301019
2017 BIRC3 is a biomarker of mesenchymal habitat of glioblastoma, and a mediator of survival adaptation in hypoxia-driven glioblastoma habitats. Scientific reports 25 28839258
2013 Anti-Apoptotic Signature in Thymic Squamous Cell Carcinomas - Functional Relevance of Anti-Apoptotic BIRC3 Expression in the Thymic Carcinoma Cell Line 1889c. Frontiers in oncology 24 24427739
2013 An intravenous (i.v.) route-compatible formulation of FL118, a survivin, Mcl-1, XIAP, and cIAP2 selective inhibitor, improves FL118 antitumor efficacy and therapeutic index (TI). American journal of translational research 23 23573360
2013 Resveratrol suppresses cell proliferation via inhibition of STAT3 phosphorylation and Mcl-1 and cIAP-2 expression in HTLV-1-infected T cells. Leukemia research 23 24090995
2023 Anastasis enhances metastasis and chemoresistance of colorectal cancer cells through upregulating cIAP2/NFκB signaling. Cell death & disease 22 37391410
2018 Identification of microRNA-124 in regulation of Hepatocellular carcinoma through BIRC3 and the NF-κB pathway. Journal of Cancer 21 30210622
2015 A critical role for cellular inhibitor of protein 2 (cIAP2) in colitis-associated colorectal cancer and intestinal homeostasis mediated by the inflammasome and survival pathways. Mucosal immunology 21 26037070
2011 Inhibition of hepatitis B virus replication by cIAP2 involves accelerating the ubiquitin-proteasome-mediated destruction of polymerase. Journal of virology 21 21865390
2010 Tristetraprolin controls the stability of cIAP2 mRNA through binding to the 3'UTR of cIAP2 mRNA. Biochemical and biophysical research communications 21 20691152
2005 cIAP2 is highly expressed in Hodgkin-Reed-Sternberg cells and inhibits apoptosis by interfering with constitutively active caspase-3. Journal of molecular medicine (Berlin, Germany) 21 16308685
2016 SHh-Gli1 signaling pathway promotes cell survival by mediating baculoviral IAP repeat-containing 3 (BIRC3) gene in pancreatic cancer cells. Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine 20 26815504
2012 cIAP2 represses IKKα/β-mediated activation of MDM2 to prevent p53 degradation. Cell cycle (Georgetown, Tex.) 20 23032264
2007 Upregulation of cIAP2 in regenerating colonocytes in ulcerative colitis. Virchows Archiv : an international journal of pathology 20 17972100
2020 H. pylori infection confers resistance to apoptosis via Brd4-dependent BIRC3 eRNA synthesis. Cell death & disease 19 32820150
2015 Neisseria gonorrhoeae Modulates Cell Death in Human Endocervical Epithelial Cells through Export of Exosome-Associated cIAP2. Infection and immunity 19 26077759
2006 Cell cycle-dependent expression of cIAP2 at G2/M phase contributes to survival during mitotic cell cycle arrest. The Biochemical journal 19 16813569

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