Publication for Birc3 and Birc2

Species	Symbol	Function*	Entrez Gene ID*	Other ID	Gene coexpression	CoexViewer
mmu	Birc3	baculoviral IAP repeat-containing 3	11796			[link]
mmu	Birc2	baculoviral IAP repeat-containing 2	11797

Pubmed ID	Priority	Text
19276372	0.98	Birc2 (cIAP1) and Birc3 (cIAP2), Amplified on Chromosome 9, Collaborate with p53 Deficiency in Mouse Osteosarcoma Progression
	0.98	Birc2 (cIAP1), and Birc3 (cIAP2) show elevated expression in mouse and human osteosarcomas.
	0.98	Birc2 (cIAP1) and Birc3 (cIAP2) are important in promoting osteosarcomagenesis.
	0.98	Birc2 and Birc3 mRNA expression in virtually all tumors (Figure 5A, Figure S6).
	0.98	Birc2 and Birc3 and is co-amplified with these anti-apoptotic genes in the chromosome 9A1 amplicon containing osteosarcomas.
	0.98	Birc2, Birc3, and Yap1 were expressed at high levels relative to osteoblasts, though Yap1 was only overexpressed in osteosarcomas with the chromosome 9A1 amplicon.
	0.98	Birc2 and Birc3 knockdown (but not in A- tumors).
	0.98	Birc2 and Birc3 expression during early stages of osteosarcoma evolution.
	0.98	Birc2 and Birc3 are potential oncogenic drivers of selection for the chromosome 9A1 amplicon and are required for A+ osteosarcoma progression, but upregulation of these two genes is not universally required for osteosarcoma progression.
	0.98	Birc2 and Birc3 expression are increased in mouse and human osteosarcomas and are required for robust growth of osteosarcomas with chromosome 9A1 amplification
	0.97	Birc2 and Birc3 also enhance cell survival, but only in osteosarcoma cells with the chromosome 9A1 amplicon.
	0.97	Birc2 and Birc3 are potential oncogenic drivers in the chromosome 9A1 amplicon.
	0.97	Birc2 can affect the TNFalpha pathway by binding and ubiquitinating the TNFR-associated factor-2 (TRAF2), whereas Birc3 preferentially binds and ubiquitinates TRAF1.
	0.97	Birc2 and high Birc3 expression contributed to tumor growth and reduced apoptosis only in osteosarcomas with the chromosome 9A1 amplicon.
	0.97	Birc2 and Birc3 may block apoptosis by impeding caspase-8 dependent autocrine TNF-alpha signaling.
	0.96	Birc2, or Birc3 resulted in reduced tumor growth when transplanted into immunodeficient recipient mice.
	0.96	Birc2 (cIAP1) and Birc3 (cIAP2) may regulate apoptotic pathways by multiple mechanisms.
	0.96	Birc2 and Birc3 during subsequent stages of tumor evolution.
	0.96	Birc2 and Birc3 levels, downregulating these genes through shRNA approaches will have profound effects on tumor growth rates.
	0.96	Birc2 and/or Birc3 occurs with some frequency during cancer progression, suggesting that treatments targeting these two gene products may provide useful therapeutic options.
	0.95	Birc2 and Birc3 enhances apoptosis and reduces tumor growth rates in amplicon positive osteosarcomas
	0.94	Birc2 (cIAP1) and Birc3 (cIAP2).
	0.94	Birc2 (cIAP1) and Birc3 (cIAP2) genes, which encode inhibitors of apoptosis (Figure 1D).
	0.93	Birc2 and Birc3 may enhance cancer cell survival have been discussed.
	0.93	Birc2 and Birc3 knockdown result in reduced tumor growth rates in A+ osteosarcoma cells, but not A- osteosarcoma cells after subcutaneous transplant in nude mice.
	0.92	Birc2 and Birc3 expression provide a selective cell survival advantage to those tumors with the 9A1 amplicon while no such advantage is provided to the amplicon negative tumors.
	0.92	Birc2 and Birc3 has been observed in esophageal cancer, chronic neutrophilic leukemia, renal cell carcinomas, B-cell lymphomas, and pancreatic cancer.
	0.92	Birc2 and Birc3 knockdown increases tumor apoptosis rates in A+ osteosarcoma cells, but not A- osteosarcoma cells after transplantation in nude mice.
	0.91	Birc2 (cIAP1) and Birc3 (cIAP2) are located near the epicenter of the chromosome 9A1 amplicon.
	0.91	Birc2 and Birc3 expression, while A- osteosarcoma growth was not dependent on Birc2 and Birc3 expression levels.
	0.90	Birc2 and Birc3 has also been observed in mouse liver cancers and human lung cancer, liver carcinomas, oral squamous cell carcinomas, medulloblastomas, glioblastomas, and pancreatic cancers.
	0.89	Birc2 and Birc3 expression, while elevated, are not as high as in the amplicon positive tumors (see Figure 5A).
	0.87	Birc2 or Birc3 shRNA-expressing A+ osteosarcoma sections contained significantly increased apoptotic cell percentages (Figure 5C), while no significant differences in apoptotic cell percentages were noted in shRNA vector transduced A- osteosarcoma sections.
	0.83	Birc2, Birc3 and Yap1 are located in the chromosome 9 amplicon about one Mb downstream of the MMP cluster.
	0.81	Birc2, Birc3 and Yap1 in osteosarcomagenesis.
	0.62	Birc2 or Birc3 shRNA-expressing A+ tumors grew significantly slower than empty vector-transduced A+ tumors (Figure 5B, upper panels).
	0.62	Birc2 and Birc3 shRNA, the amplicon negative tumors, dependent on other anti-apoptotic genes for tumor cell survival, will not be affected.
26094954	0.98	BIRC2 and BIRC3 are closely related members of the inhibitor of apoptosis (IAP) family of proteins and play pivotal roles in regulation of nuclear factor-kappaB (NF-kappaB) signaling and apoptosis.
	0.98	BIRC2 and BIRC3 have been frequently detected in lymphoid malignancies, with such genetic alterations being thought to contribute to carcinogenesis through activation of the noncanonical NF-kappaB signaling pathway.
	0.98	BIRC2 (also known as cIAP1) and BIRC3 (also known as cIAP2), two closely related members of the IAP family, catalyze the ubiquitylation of RIPK1 in a manner dependent on their RING finger domains.
	0.97	BIRC2 and BIRC3 mutations are also present in a wide range of epithelial tumors and that most such nonsense or frameshift mutations confer direct transforming potential.
	0.97	BIRC2 and BIRC3 mutants that is, at least in part, unrelated to the ability of these mutants to regulate NF-kappaB signaling.
	0.96	BIRC2 and BIRC3 genes have been identified in lymphoid malignancies.
	0.94	BIRC2 to activate NF-kappaB, such effect was marginal for some mutants and others even suppressed NF-kappaB (Fig.4c), indicative of an NF-kappaB-independent transformation mechanism for BIRC2 as for BIRC3.
	0.92	BIRC3, the transforming ability of BIRC2(H588A) was attenuated but not abolished in cells depleted of Nik (Fig.4d).
	0.87	BIRC2 and BIRC3 mutants independent of nuclear factor-kappaB-activating potential
	0.80	BIRC3, a catalytic-null mutant of BIRC2, BIRC2(H588A), also manifested transforming potential.
27830706	0.98	Birc2 and Birc3, and exert anti-apoptotic effects.
	0.98	Birc2 and Birc3 are induced by NF-kappaB signalling and mediate resistance against TNF-induced apoptosis.
	0.97	Birc2(c-Iap1), Birc3(c-Iap2) and Pik3r1 was increased by TNF treatment and decreased by Rela deletion (Fig. 5b).
	0.97	Birc2, Birc3, Pik3r1, Adamts5 and Hif2a were decreased, and their mRNA levels in Cre-overexpressing Relafl/+ chondrocytes were significantly higher than those in Cre-overexpressing Relafl/fl chondrocytes (Figs 5b, 7e and 8a).
	0.86	Birc2 and Birc3 were restored by the Rela adenovirus at 20 multiplicity of infection, whereas the restoration of Pik3r1, Adamts5 and Hif2a required an multiplicity of infection of 100 (Fig. 8c).
26122662	0.98	BIRC2 and BIRC3 elicits NIK accumulation, which leads to proteasome-dependent processing of p100 into p52 and hence activates the noncanonical NF-kappaB pathway.
	0.98	BIRC2 and BIRC3 in their beta cells (betaBIRC2/3) exhibit islet-intrinsic NIK hyperactivation, as indicated by increased p100 processing (Fig. 6 A) with impaired glucose tolerance and reduced insulin secretion in a DIO model (Fig. 6, B and C).
	0.98	BIRC2-BIRC3 E3 ligase complex are required to provide the beta cell protective circuit that reigns in the deleterious activation of NIK, which suggests that firm regulation of NIK in beta cells is essential to control glucose sensing and insulin secretion.
	0.96	BIRC2 and BIRC3 degradation, we hypothesized genetic ablation of BIRC2 and BIRC3 in beta cells would trigger a beta cell defect.
18997794	0.98	Birc2 and Birc3 genes.
	0.97	cIAP1 in Birc3-/- cells, knockdown of cIAP2 in Birc2-/- cells or knockdown of both in wild-type cells results in NIK accumulation and noncanonical NF-kappaB activation.
19103199	0.98	BIRC-2 (and BIRC-3), factors that via their binding to TRAF-1 and TRAF-2 can induce expression of NF-kbeta and subsequently reduced caspase activity.
	0.98	Birc2 and Birc3 are highly reduced in the lacrimal glands of mice at their later ages and this potentially could promote apoptosis seen at the later stages of SjS. On the other hand, IFN-gamma, GM-CSF, IL-2, and IL-18 can up-regulate expression of caspase-8 leading to activation of caspase-3.
24072531	0.98	inhibitor of apoptosis protein 2 (cIAP2 [also known as HIAP1 or BIRC3]) is a member of the IAP gene family involved in programmed cell death regulation.
	0.94	inhibitor of apoptosis protein 2 (cIAP2) is predicted to participate in atherosclerosis; however, its direct role in atherosclerosis development has not been investigated.
26365200	0.98	BIRC2, BIRC3) match previous results on the role of ATRA in inducing apoptosis.
	0.98	BIRC2, BIRC3), suggesting that exposure to ATRA leads to lesser spheroid contraction via increased apoptosis.
28352235	0.98	BIRC2 and BIRC3 nor the combined knockdowns with XIAP modifies the cell response to FasL stimulation.
	0.87	c-IAP1/BIRC2 was slightly increased in fibroblasts (12 and 10%, respectively); while the expression of IAP2/BIRC3 was 11% lower than in resting Cav-null fibroblasts (Figure 6A, red boxes) when compared to ECs and EpCs.
29980757	0.98	Birc2, Birc3, Birc5 and Xiap) were upregulated in DEN/TAA/HFD livers compared to control, and some of these were also upregulated in DEN/TAA/HFD compared to DEN/TAA (Fig. 5A,F; Table 1).
	0.96	Birc2, Birc3, Birc5 and Xiap, were more pronounced in DEN/TAA/HFD treated than in DEN/TAA treated mice.
18997792	0.98	cIAP1 (BIRC2) and cIAP2 (BIRC3) are deleted, cells exhibit NIK accumulation and constitutive p100 processing.
21931631	0.98	cIAP1 and cIAP2 (encoded by the genes BIRC3 and BIRC2), which were identified as interactors of both TBK1 and IKK-I (Fig. 1C), are E3 ligases which were originally found associated with TRAF1 and TRAF2 and function in the TNFR1 pathway.
23674823	0.98	cellular inhibitor of apoptosis 1 (cIAP1) and cIAP2 (collectively known as cIAP1/2).
25607459	0.98	BIRC2, BIRC3, and BIRC4) in BMDMs has been reported to result in spontaneous NLRP3 inflammasome activation by a RIPK3 (receptor-interacting protein kinase 3)-dependent mechanism.
26046700	0.98	Birc2, Birc3 and Traf2 are known for their anti-apoptotic effects.
28476895	0.98	cIAP1 (Birc2) and cIAP2 (Birc3), SMAC mimetics foster degradation of cIAPs to activate apoptosis.
29321275	0.98	Birc2 (cIAP1), A20, Traf3, Traf1, and Birc3 (cIAP2) as well as Cd40 itself, were expressed highly in mature tDCs relative to immature tDCs (Fig. 7A).
29574534	0.98	inhibitor of apoptosis protein 1 (cIAP1 or BIRC2), enhancing DR5-related signaling and lipoapoptosis (Fig. 2).
31396572	0.98	cIAP1 (Birc2), cIAP2 (Birc3), and A20 (Tnfaip3) (Fig. 5e), but not of XIAP (Birc4) and Survivin (Birc5) (Supplementary Fig. 8A), were significantly upregulated during pregnancy in TRAF6-He luminal cells.
31554891	0.98	cIAP1 (Birc2) were upregulated in Nfkb2-/- Tregs (Fig. 8C).
32180561	0.98	Birc2 (Ciap1) and Tnfaip3 (also known as A20), two anti-apoptotic proteins that prevent cell death downstream of inflammatory signaling.
28194015	0.97	Birc2 and Birc3, which encode IAP family of proteins that inhibit apoptosis (Fig. 5a, left).
	0.93	Birc2, Birc3, Yap1) from this region in almost all profiled Type 1 tumours (for example, E2, E4, E5, E9, TB208, TB209, TB239-2), but not in the Type 2 tumour E8 (Fig. 5b, top).
	0.81	Birc2, Birc3 and Yap1 were also found previously in mammary tumours developed in other breast cancer mouse models with p53 deficiency.
28486401	0.97	cellular inhibitor of apoptosis 1 (cIAP1), cellular inhibitor of apoptosis 2 (cIAP2) and linear ubiquitin chain assembly complex (LUBAC).
29930103	0.97	cIAP1 protein expression are likely due to posttranscriptional mechanisms, because mRNA levels of BIRC2 (cIAP1), BIRC3 (cIAP2), and CFLAR (cFLIP) were greater in A20FL/FLABIN-1FL/FL villin-ER/Cre+ IECs than in normal or single-mutant cells (Fig. 4 B).
18187509	0.96	Birc2 and Birc3.
22682366	0.96	Birc2 and Birc3 have been observed in mouse liver and human lung cancers, liver carcinoma, oral squamous cell carcinoma, medulloblastoma, glioblastoma, and pancreatic cancer.
23702978	0.96	inhibitor of apoptosis protein 1 (IAP1; also known as BIRC3) and IAP2 (also known as BIRC2) (REF).
27549026	0.96	Baculoviral IAP repeat-containing protein 2 (also known as C-IAP1) and Baculoviral IAP repeat-containing protein 3 (also known as C-IAP2).
22332634	0.94	c-IAP1 and c-IAP2, Birc2 and Birc3 respectively, are in close proximity to the caspase 11 gene on mouse chromosome 9, and, as such, mice deficient in c-IAP1 and c-IAP2 also potentially carry the mutation in the caspase 11 locus.
27314066	0.94	baculoviral IAP repeat containing 2 (BIRC2, best known as cIAP1) and BIRC3 (best known as cIAP2), which are known to display high homology and functional redundancy.
26840261	0.88	BIRC2 expression, as BIRC3 levels were not changed by AMPA treatment.
	0.86	Baculoviral IAP Repeat Containing 2 (BIRC2, also called cIAP1), but did not change the expression of BIRC3 (also called cIAP2) proteins.
28422189	0.88	BIRC2, BIRC3 and XIAP knockout murine IBD models.
30442927	0.85	BIRC2, BIRC3, and cFLIP), which were important molecules of TLRs signaling pathway, in JNK-depleted macrophages and found that they exhibited no significant difference compared with control macrophages (Fig. 6f).
30778285	0.85	cIAP1) and inhibitor of apoptosis protein 2 (cIAP2).
20703218	0.83	BIRC2 (also known as cIAP1), BIRC3 (also known as cIAP2) and BCL2L1 (also known as Bcl-XL).
31959748	0.71	Birc2, Birc3 and Yap1, also localised in the amplified region, showed some level of over-expression and may also be functionally significant.
31818366	0.67	BIRC2/CIAP1, and MDM2), but not others (PARK2, XIAP, and BIRC3/CIAP2), irrespective of the presence of the RING domain.
21317297	0.55	Birc2/Birc3), and placenta and embryonic expression gene onco-fetal gene (Pem).