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BIRC2 (baculoviral IAP repeat-containing 2)

Identity

Other namesAPI1
C-IAP1
HIAP-2
HIAP2
Hiap-2
IAP2
MIHB
RNF48
cIAP1
hiap-2
HGNC (Hugo) BIRC2
LocusID (NCBI) 329
Location 11q22.2
Location_base_pair Starts at 102217913 and ends at 102249401 bp from pter ( according to hg19-Feb_2009)  [Mapping]

DNA/RNA

 
Description 31,436 bp, 9 exons.
Transcription 3,753 bp mRNA.

Protein

 
Description 618 amino acids. The protein contains three motifs, i.e., BIR (Baculoviral Inhibitor of Apoptosis Repeat) domain, RING (Really Interesting New Gene)-finger domain, and CARD (Caspase Recruitment Domain).
Expression Wide, highly expressed in large intestine, lung, endometrium, bladder and salivary gland.
Localisation Cytoplasmic and/or nucleus.
Function Inhibition of apoptosis by preventing the proteolytic processing of procaspase-3, procaspase-6, and procaspase-7, by inhibiting the cytochrome C-induced activation of procaspase-9; by binding to tumor necrosis factor receptor-associated factor II (TRAF2) and enhancing TRAF2-induced NF-kappaB activity that protects TRAF2 from ubiquitination in cells; by promoting the proteasome-dependent degradation of Smac/DIABLO through E3 ubiquitin ligase activity of their RING finger domains; and by direct ubiquitination of RIP1 in cancer cells and its association with the prosurvival kinase TAK1 (TGF-beta-activated kinase 1) (LaCasse et al., 2008).
Homology Mouse, Rat.

Mutations

Note Not found.

Implicated in

Entity Malignant lymphoma
Note All cIAP1/BIRC2, cIAP2 and XIAP were expressed in most of 240 non-Hodgkin lymphoma and all 40 Hodgkin lymphoma cell lines.
In non-Hodgkin lymphomas, cIAP1 was expressed in 73%, cIAP2 in 48% and XIAP in 15%. cIAP was positive in all precursor B-cell lymphoblastic lymphoma/leukemia and nodal marginal zone B-cell lymphoma, over 90% of follicular lymphoma and diffuse large B-cell lymphoma, and approximately 50 to 60% of myeloma, Burkitt lymphoma , lymphoplasmacytic lymphoma, small lymphocytic lymphoma/chronic lymphocytic leukemia, extranodal marginal zone B-cell lymphoma of mucosa associated lymphoid tissue (MALT-lymphoma), splenic marginal zone lymphoma, and mantle cell lymphoma.
In Hodgkin lymphomas, cIAP was positive in 75%, and were not correlated with histologic type (Akyurek et al., 2006). Treatment of diffuse large B-cell lymphoma cells with bortezomib caused apoptosis via involving the mitochondrial pathway and activation of caspases, and finally down-regulate the expression of cIAP1, XIAP and survivin (Uddin et al., 2008). Among multiple myeloma patients with increased multidrug-resistant (MDR) 1 expression after chemotherapy, those with a poor outcome exhibited significant increase in survivin, cIAP1, cIAP2, and XIAP expression by chemotherapy compared with those with a good prognosis. Similarly, in the lung resistance protein (LRP) expression-increased group, patients with a poor outcome showed significant increase of cIAP1 and cIAP2 expression compared with those with longer survival (Nakagawa et al., 2006). An integrated analysis of high-density oligonucleotide array CGH and gene expression profiling data from 155 multiple myeloma samples identified a promiscuous array of abnormalities contributing to the dysregulation of NF-KB in approximately 20% of patients. Mutations in 10 genes causing the inactivation of TRAF2, TRAF3, CYLD, cIAP1/cIAP2 and the activation of NF-kappaB1, NF-kappaB2, CD40, LTBR, TACI, and NIK that result primarily in constitutive activation of the noncanonical NF-KB pathway, with the single most common abnormality being inactivation of TRAF3 (Keats et al., 2007).
  
Entity Myelodysplastic syndrome
Note Overexpression of mRNA for survivin, cIAP1, NAIP and XIAP was significant in myelodysplastic syndrome bone marrow cells compared with control samples. However, the expression of mRNA for survivin, cIAP1 and cIAP2 exhibited a remarkable decrease after the development of overt leukemia (Yamamoto et al., 2004).
  
Entity Squamous cell carcinoma of head and neck (HNSCC)
Note Nuclear cIAP-1 expression was positive in 30% of HNSCC, was correlated with lymph node metastasis and advanced disease stage, and tend to be correlated with poor patient prognosis. Nuclear cIAP-1 expression was inversely correlated with caspase-3 expression, but was correlated with Smac/DIABLO expression. Nuclear cIAP-1 expression appears to be a useful marker for predicting poor patient prognosis in HNSCCs, and may play roles in HNSCC through the signaling pathway mediated by Smac/DIABLO and caspase-3 (Tanimoto et al., 2005). Nuclear, cytoplasmic and concurrent cIAP-1 immunoreactions were significantly correlated with lymph node metastasis in tongue SCCs. Concurrent cIAP-1 expression was inversely correlated with caspase-3, but was positively correlated with Ki-67 expression. Both nuclear and cytoplasmic patterns of cIAP-1 expression was useful markers for predicting cervical lymph node metastasis in tongue SCC (Qi et al., 2008).
  
Entity Squamous cell carcinoma (SCC) of esophagus
Note High copy-number amplification at 11q21-q23 was identified in cell lines derived from esophageal SCCs using comparative genomic hybridization. Only cIAP1 was consistently overexpressed in cell lines that showed amplification. cIAP1 protein was overexpressed in the primary tumors from which those cell lines had been established. cIAP1 is likely to be a target for 11q21-23 amplification and may be involved in the progression of esophageal SCC (Imoto et al., 2001).
  
Entity Squamous cell carcinoma (SCC) of uterine cervix
Note In the 2 of 9 cell lines of cervical SCC showed amplification and consistent overexpression of cIAP1, as well as significant resistance to radiation-induced cell death as compared with cell lines showing no cIAP1 amplification. Both overall survival and local recurrence-free survival rates were significantly lower among patients with tumors showing high levels of nuclear cIAP1 staining than among patients whose tumors revealed little or no nuclear cIAP1. Multivariate analyses showed nuclear cIAP1 staining to be an independent predictive factor for local recurrence-free survival after radiotherapy among patients with cervical SCC (Imoto et al., 2002).
  
Entity Adenoid cystic carcinoma of lacrymal gland
Note Expression of cIAP1, cIAP2, XIAP and survivin was higher in adenoid cystic carcinoma than in pleomorphic adenoma of the lacrymal gland (Liao et al., 2009).
  
Entity Nasopharyngeal carcinoma (NPC)
Note Among the IAPs family, only trancription of survivin, HIAP-1 and HIAP-2/BIRC2 was consistently up-regulated in nasopharyngeal carcinoma (NPC) and metastatic NPC tissues. Immunohistochemical staining showed that their proteins were more predominantly expressed in tumor cells nests. Survivin, HIAP-1 and HIAP-2 were upregulated by interleukin-1 alpha stimulation or EBV infection, and subsequently resulted in triggering rapid proliferation of NPC (Chua et al., 2008).
  
Entity Lung cancer
Note Amplification of chromosome 11q22 was detected in primary tumors and lung cancer cell lines of both non-small cell lung cancer and small cell lung cancer. Gene localized in this region included cIAP1 and cIAP2. Immunohistochemistry and western blot analysis identified cIAP1 and cIAP2 as potential oncogenes in this region as both were overexpressed in multiple lung cancers (Dai et al., 2003).
  
Entity Malignant pleural mesothelioma
Note IAP-1 was overexpressed in malignant pleural mesothelioma and is responsible for a large degree of the resistance of cultured mesothelioma cells to cisplatin. Levels of circulating TNF-alpha were significantly higher in mesothelioma patients prior to surgical tumor debulking compared with those after surgery. TNF-alpha could increase mRNA and protein levels of IAP-1, IAP-2 and XIAP. IAP gene expression levels were increased concomitantly with translocation to the nucleus of the TNF-responsive transcription factor NF-KB (Gordon et al., 2007).
  
Entity Renal cell carcinoma
Note Overexpression of cIAP1 and cIAP2 occurred in most renal cell carcinoma specimens, but 20% of the patients had lower cIAP levels in malignant than in normal tissue. The cIAP1 expression correlated with the tumor stage, levels being higher in pT1 tumors than in advanced pathological stages. Decreased cIAP1 expression in renal cell carcinoma relative to paired normal samples predicted an abbreviated time to recurrence and tumor-specific survival irrespectively of the tumor stage and grade. The prognostic effect of cIAP1 was most pronounced in patients with pT3 disease. The results of uni- and multivariate analyses suggested a prognostic value of cIAP1 expression for renal cell carcinoma patients, downregulation indicating an aggressive, potentially lethal phenotype (Kempkensteffen et al., 2007).
  
Entity Pancreatic neoplasms
Note cIAP1 expression was constantly high in non-neoplastic pancreatic tissues, in pancreatic intraepithelial neoplasia lesions, as well as in a subset of primary and metastatic pancreatic ductal adenocarcinomas, and a preferential cytoplasmic localisation was observed in the tumor tissues. cIAP expression was rare in a cystic tumors. Survival analyses revealed a shorter survival in patients with cIAP1/cIAP2-positive tumors (Esposito et al., 2007).
  
Entity Endometrial cancer
Note cIAP-1 expression was high in endometrial cancer cells expressing phospho-Akt. Akt phosphorylation decreased and apoptosis was strongly increased in PTEN-mutated endometrial cancer cells in the presence of phosphatidylinositol 3 kinase (PI3-K) inhibitor which was accompanied by a down-regulation of cIAP-1. Overexpression of Akt using a constitutively active Akt expression vector resulted in an up-regulation of cIAP-1 expression. Akt regulated endometrial cancer cell survival through the up-regulation of cIAP-1 (Gagnon et al., 2003).
  
Entity Various cancer cell lines
Note cIAP1 and XIAP were expressed in most cancer lines analised, with substantial variability in their relative levels. Higher levels of cIAP1 protein were associated with resistance to several anticancer drugs (Tamm et al., 2000). IAPs were induced by NF-KB or v-Rel in multiple cell lines and conversely, HIAP1 and HIAP2 activated NF-kappaB possibly forming a positive feed-back loop (LaCasse et al., 1998). cIAP1 and cIAP2 promoted cancer cell survival by functioning as E3 ubiquitin ligases that maintain constitutive ubiquitination of the RIP1 adaptor protein (Bertrand et al., 2008).
  

External links

Nomenclature
HGNC (Hugo)BIRC2   590
Cards
AtlasBIRC2ID795ch11q22
Entrez_Gene (NCBI)BIRC2  329  baculoviral IAP repeat containing 2
GeneCards (Weizmann)BIRC2
Ensembl (Hinxton)ENSG00000110330 [Gene_View]  chr11:102217913-102249401 [Contig_View]  BIRC2 [Vega]
AceView (NCBI)BIRC2
Genatlas (Paris)BIRC2
WikiGenes329
SOURCE (Princeton)NM_001166 NM_001256163 NM_001256166
Genomic and cartography
GoldenPath (UCSC)BIRC2  -  11q22.2   chr11:102217913-102249401 +  11q22   [Description]    (hg19-Feb_2009)
EnsemblBIRC2 - 11q22 [CytoView]
Mapping of homologs : NCBIBIRC2 [Mapview]
OMIM601712   
Gene and transcription
Genbank (Entrez)AK225856 AK303197 AK313446 BC016174 BC028578
RefSeq transcript (Entrez)NM_001166 NM_001256163 NM_001256166
RefSeq genomic (Entrez)AC_000143 NC_000011 NC_018922 NT_033899 NW_001838042 NW_004929381
Consensus coding sequences : CCDS (NCBI)BIRC2
Cluster EST : UnigeneHs.731943 [ NCBI ]
CGAP (NCI)Hs.731943
Alternative Splicing : Fast-db (Paris)GSHG0005209
Alternative Splicing GalleryENSG00000110330
Gene ExpressionBIRC2 [ NCBI-GEO ]     BIRC2 [ SEEK ]   BIRC2 [ MEM ]
Protein : pattern, domain, 3D structure
UniProt/SwissProtQ13490 (Uniprot)
NextProtQ13490  [Medical]
With graphics : InterProQ13490
Splice isoforms : SwissVarQ13490 (Swissvar)
Catalytic activity : Enzyme6.3.2.- [ Enzyme-Expasy ]   6.3.2.-6.3.2.- [ IntEnz-EBI ]   6.3.2.- [ BRENDA ]   6.3.2.- [ KEGG ]   
Domaine pattern : Prosite (Expaxy)BIR_REPEAT_1 (PS01282)    BIR_REPEAT_2 (PS50143)    CARD (PS50209)    ZF_RING_1 (PS00518)    ZF_RING_2 (PS50089)   
Domains : Interpro (EBI)BIR    CARD    DEATH-like_dom    Znf_RING   
Related proteins : CluSTrQ13490
Domain families : Pfam (Sanger)BIR (PF00653)    CARD (PF00619)   
Domain families : Pfam (NCBI)pfam00653    pfam00619   
Domain families : Smart (EMBL)BIR (SM00238)  CARD (SM00114)  RING (SM00184)  
DMDM Disease mutations329
Blocks (Seattle)Q13490
PDB (SRS)1QBH    2L9M    3D9T    3D9U    3M1D    3MUP    3OZ1    3T6P    3UW4    4EB9    4HY4    4HY5   
PDB (PDBSum)1QBH    2L9M    3D9T    3D9U    3M1D    3MUP    3OZ1    3T6P    3UW4    4EB9    4HY4    4HY5   
PDB (IMB)1QBH    2L9M    3D9T    3D9U    3M1D    3MUP    3OZ1    3T6P    3UW4    4EB9    4HY4    4HY5   
PDB (RSDB)1QBH    2L9M    3D9T    3D9U    3M1D    3MUP    3OZ1    3T6P    3UW4    4EB9    4HY4    4HY5   
Human Protein AtlasENSG00000110330
Peptide AtlasQ13490
HPRD03419
IPIIPI00013418   IPI00984575   IPI00975834   IPI00977511   IPI00976514   IPI00984201   IPI00984756   IPI00980653   
Protein Interaction databases
DIP (DOE-UCLA)Q13490
IntAct (EBI)Q13490
FunCoupENSG00000110330
BioGRIDBIRC2
InParanoidQ13490
Interologous Interaction database Q13490
IntegromeDBBIRC2
STRING (EMBL)BIRC2
Ontologies - Pathways
Ontology : AmiGOprotein polyubiquitination  placenta development  toll-like receptor signaling pathway  MyD88-independent toll-like receptor signaling pathway  transcription coactivator activity  ubiquitin-protein ligase activity  protein binding  nucleus  cytosol  transcription, DNA-templated  regulation of transcription, DNA-dependent  apoptotic process  cellular component disassembly involved in execution phase of apoptosis  cell surface receptor signaling pathway  zinc ion binding  cytoplasmic side of plasma membrane  regulation of toll-like receptor signaling pathway  toll-like receptor 3 signaling pathway  toll-like receptor 4 signaling pathway  CD40 receptor complex  TRIF-dependent toll-like receptor signaling pathway  NIK/NF-kappaB cascade  regulation of RIG-I signaling pathway  regulation of cell proliferation  regulation of apoptotic process  negative regulation of apoptotic process  negative regulation of apoptotic process  positive regulation of I-kappaB kinase/NF-kappaB cascade  proteasome-mediated ubiquitin-dependent protein catabolic process  innate immune response  regulation of innate immune response  regulation of cell differentiation  protein N-terminus binding  regulation of inflammatory response  regulation of cell cycle  regulation of necroptotic process  necroptotic process  regulation of nucleotide-binding oligomerization domain containing signaling pathway  regulation of cysteine-type endopeptidase activity  
Ontology : EGO-EBIprotein polyubiquitination  placenta development  toll-like receptor signaling pathway  MyD88-independent toll-like receptor signaling pathway  transcription coactivator activity  ubiquitin-protein ligase activity  protein binding  nucleus  cytosol  transcription, DNA-templated  regulation of transcription, DNA-dependent  apoptotic process  cellular component disassembly involved in execution phase of apoptosis  cell surface receptor signaling pathway  zinc ion binding  cytoplasmic side of plasma membrane  regulation of toll-like receptor signaling pathway  toll-like receptor 3 signaling pathway  toll-like receptor 4 signaling pathway  CD40 receptor complex  TRIF-dependent toll-like receptor signaling pathway  NIK/NF-kappaB cascade  regulation of RIG-I signaling pathway  regulation of cell proliferation  regulation of apoptotic process  negative regulation of apoptotic process  negative regulation of apoptotic process  positive regulation of I-kappaB kinase/NF-kappaB cascade  proteasome-mediated ubiquitin-dependent protein catabolic process  innate immune response  regulation of innate immune response  regulation of cell differentiation  protein N-terminus binding  regulation of inflammatory response  regulation of cell cycle  regulation of necroptotic process  necroptotic process  regulation of nucleotide-binding oligomerization domain containing signaling pathway  regulation of cysteine-type endopeptidase activity  
Pathways : BIOCARTARole of Mitochondria in Apoptotic Signaling [Genes]    HIV-I Nef: negative effector of Fas and TNF [Genes]    Caspase Cascade in Apoptosis [Genes]    Induction of apoptosis through DR3 and DR4/5 Death Receptors [Genes]   
Pathways : KEGGNF-kappa B signaling pathway    Ubiquitin mediated proteolysis    Apoptosis    Hippo signaling pathway    Focal adhesion    NOD-like receptor signaling pathway    TNF signaling pathway    Toxoplasmosis    Pathways in cancer    Small cell lung cancer   
REACTOMEBIRC2
Protein Interaction DatabaseBIRC2
Wikipedia pathwaysBIRC2
Gene fusion - rearrangments
Polymorphisms : SNP, mutations, diseases
SNP Single Nucleotide Polymorphism (NCBI)BIRC2
SNP (GeneSNP Utah)BIRC2
SNP : HGBaseBIRC2
Genetic variants : HAPMAPBIRC2
1000_GenomesBIRC2 
ICGC programENSG00000110330 
Somatic Mutations in Cancer : COSMICBIRC2 
CONAN: Copy Number AnalysisBIRC2 
Mutations and Diseases : HGMDBIRC2
OMIM601712   
GENETestsBIRC2
Disease Genetic AssociationBIRC2
Huge Navigator BIRC2 [HugePedia]  BIRC2 [HugeCancerGEM]
Genomic VariantsBIRC2  BIRC2 [DGVbeta]
Exome VariantBIRC2
dbVarBIRC2
ClinVarBIRC2
snp3D : Map Gene to Disease329
General knowledge
Homologs : HomoloGeneBIRC2
Homology/Alignments : Family Browser (UCSC)BIRC2
Phylogenetic Trees/Animal Genes : TreeFamBIRC2
Chemical/Protein Interactions : CTD329
Chemical/Pharm GKB GenePA25359
Clinical trialBIRC2
Cancer Resource (Charite)ENSG00000110330
Other databases
Probes
Litterature
PubMed184 Pubmed reference(s) in Entrez
CoreMineBIRC2
iHOPBIRC2

Bibliography

The inhibitors of apoptosis (IAPs) and their emerging role in cancer.
LaCasse EC, Baird S, Korneluk RG, MacKenzie AE.
Oncogene. 1998 Dec 24;17(25):3247-59.
PMID 9916987
 
Expression and prognostic significance of IAP-family genes in human cancers and myeloid leukemias.
Tamm I, Kornblau SM, Segall H, Krajewski S, Welsh K, Kitada S, Scudiero DA, Tudor G, Qui YH, Monks A, Andreeff M, Reed JC.
Clin Cancer Res. 2000 May;6(5):1796-803.
PMID 10815900
 
Identification of cIAP1 as a candidate target gene within an amplicon at 11q22 in esophageal squamous cell carcinomas.
Imoto I, Yang ZQ, Pimkhaokham A, Tsuda H, Shimada Y, Imamura M, Ohki M, Inazawa J.
Cancer Res. 2001 Sep 15;61(18):6629-34.
PMID 11559525
 
Expression of cIAP1, a target for 11q22 amplification, correlates with resistance of cervical cancers to radiotherapy.
Imoto I, Tsuda H, Hirasawa A, Miura M, Sakamoto M, Hirohashi S, Inazawa J.
Cancer Res. 2002 Sep 1;62(17):4860-6.
PMID 12208731
 
A comprehensive search for DNA amplification in lung cancer identifies inhibitors of apoptosis cIAP1 and cIAP2 as candidate oncogenes.
Dai Z, Zhu WG, Morrison CD, Brena RM, Smiraglia DJ, Raval A, Wu YZ, Rush LJ, Ross P, Molina JR, Otterson GA, Plass C.
Hum Mol Genet. 2003 Apr 1;12(7):791-801.
PMID 12651874
 
Akt activity in endometrial cancer cells: regulation of cell survival through cIAP-1.
Gagnon V, St-Germain ME, Parent S, Asselin E.
Int J Oncol. 2003 Sep;23(3):803-10.
PMID 12888921
 
Expression of IAP family proteins in myelodysplastic syndromes transforming to overt leukemia.
Yamamoto K, Abe S, Nakagawa Y, Suzuki K, Hasegawa M, Inoue M, Kurata M, Hirokawa K, Kitagawa M.
Leuk Res. 2004 Nov;28(11):1203-11.
PMID 15380346
 
Nuclear expression of cIAP-1, an apoptosis inhibiting protein, predicts lymph node metastasis and poor patient prognosis in head and neck squamous cell carcinomas.
Tanimoto T, Tsuda H, Imazeki N, Ohno Y, Imoto I, Inazawa J, Matsubara O.
Cancer Lett. 2005 Jun 16;224(1):141-51.
PMID 15911110
 
Expression of inhibitor of apoptosis proteins in B-cell non-Hodgkin and Hodgkin lymphomas.
Akyurek N, Ren Y, Rassidakis GZ, Schlette EJ, Medeiros LJ.
Cancer. 2006 Oct 15;107(8):1844-51.
PMID 16983704
 
IAP family protein expression correlates with poor outcome of multiple myeloma patients in association with chemotherapy-induced overexpression of multidrug resistance genes.
Nakagawa Y, Abe S, Kurata M, Hasegawa M, Yamamoto K, Inoue M, Takemura T, Suzuki K, Kitagawa M.
Am J Hematol. 2006 Nov;81(11):824-31.
PMID 16929535
 
Overexpression of cellular inhibitor of apoptosis protein 2 is an early event in the progression of pancreatic cancer.
Esposito I, Kleeff J, Abiatari I, Shi X, Giese N, Bergmann F, Roth W, Friess H, Schirmacher P.
J Clin Pathol. 2007 Aug;60(8):885-95. Epub 2006 Jun 14.
PMID 16775116
 
Inhibitor of apoptosis proteins are regulated by tumour necrosis factor-alpha in malignant pleural mesothelioma.
Gordon GJ, Mani M, Mukhopadhyay L, Dong L, Yeap BY, Sugarbaker DJ, Bueno R.
J Pathol. 2007 Mar;211(4):439-46.
PMID 17253597
 
Promiscuous mutations activate the noncanonical NF-kappaB pathway in multiple myeloma.
Keats JJ, Fonseca R, Chesi M, Schop R, Baker A, Chng WJ, Van Wier S, Tiedemann R, Shi CX, Sebag M, Braggio E, Henry T, Zhu YX, Fogle H, Price-Troska T, Ahmann G, Mancini C, Brents LA, Kumar S, Greipp P, Dispenzieri A, Bryant B, Mulligan G, Bruhn L, Barrett M, Valdez R, Trent J, Stewart AK, Carpten J, Bergsagel PL.
Cancer Cell. 2007 Aug;12(2):131-44.
PMID 17692805
 
Expression parameters of the inhibitors of apoptosis cIAP1 and cIAP2 in renal cell carcinomas and their prognostic relevance.
Kempkensteffen C, Hinz S, Christoph F, Kollermann J, Krause H, Schrader M, Schostak M, Miller K, Weikert S.
Int J Cancer. 2007 Mar 1;120(5):1081-6.
PMID 17154176
 
cIAP1 and cIAP2 facilitate cancer cell survival by functioning as E3 ligases that promote RIP1 ubiquitination.
Bertrand MJ, Milutinovic S, Dickson KM, Ho WC, Boudreault A, Durkin J, Gillard JW, Jaquith JB, Morris SJ, Barker PA.
Mol Cell. 2008 Jun 20;30(6):689-700.
PMID 18570872
 
Regulation of IAPs gene family by interleukin-1 alpha and Epstein-Barr virus in nasopharyngeal carcinoma.
Chua HH, Yeh TH, Wang YP, Sheen TS, Shew JY, Huang YT, Tsai CH.
Head Neck. 2008 Dec;30(12):1575-85.
PMID 18798303
 
IAP-targeted therapies for cancer.
LaCasse EC, Mahoney DJ, Cheung HH, Plenchette S, Baird S, Korneluk RG.
Oncogene. 2008;27(48):6252-75.
PMID 18931692
 
Expression of cIAP-1 correlates with nodal metastasis in squamous cell carcinoma of the tongue.
Qi S, Mogi S, Tsuda H, Tanaka Y, Kozaki K, Imoto I, Inazawa J, Hasegawa S, Omura K.
Int J Oral Maxillofac Surg. 2008 Nov;37(11):1047-53. Epub 2008 Jul 14.
PMID 18621506
 
S-phase kinase protein 2 is an attractive therapeutic target in a subset of diffuse large B-cell lymphoma.
Uddin S, Hussain A, Ahmed M, Belgaumi A, Al-Dayel F, Ajarim D, Bavi P, Al-Kuraya KS.
J Pathol. 2008 Dec;216(4):483-94.
PMID 18850583
 
Expression patterns and prognostic significance of inhibitor of apoptosis proteins in adenoid cystic carcinoma and pleomorphic adenoma of lachrymal gland.
Liao Y, Zeng H, Wang X, Huang Y, Chen N, Ge B, Tang L, Luo Q.
Exp Eye Res. 2009 Jan;88(1):4-11. Epub 2008 Oct 9.
PMID 18955046
 
REVIEW articlesautomatic search in PubMed
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Contributor(s)

Written06-2009Akiko Maeshima, Hitoshi Tsuda
Clinical Laboratory Division, National Cancer Center Hospital, Tokyo, Japan

Citation

This paper should be referenced as such :
Maeshima A, Tsuda H . BIRC2 (baculoviral IAP repeat-containing 2). Atlas Genet Cytogenet Oncol Haematol. June 2009 .
URL : http://AtlasGeneticsOncology.org/Genes/BIRC2ID795ch11q22.html

The various updated versions of this paper are referenced and archived by INIST as such :
http://documents.irevues.inist.fr/bitstream/2042/44749/1/06-2009-BIRC2ID795ch11q22.pdf   [ Bibliographic record ]

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indexed on : Wed Apr 16 11:33:42 CEST 2014

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