Atlas of Genetics and Cytogenetics in Oncology and Haematology
BIN1 (bridging integrator 1)
| Identity |
| Other names | AMPH-II |
| AMPH2 | |
| AMPHL | |
| ALP | |
| DKFZp547F068 | |
| MGC10367 | |
| SH3P9 | |
| HGNC (Hugo) | BIN1 |
| LocusID (NCBI) | 274 |
| Location | 2q14.3 |
| Location_base_pair | Starts at 127805599 and ends at 127864903 bp from pter ( according to hg19-Feb_2009) [Mapping] |
| DNA/RNA |
| Description | The human BIN1 gene is encoded by at least 16 exons spanning at least 59,258 bps at chromosome 2q14-2q21 (nucleotides 127,522,078-127,581,334). The murine Bin1 gene is similarly sized but localized to a syntenic locus on mouse chromosome 8. |
| Transcription | The Bin1 promoter is rich in CpG methylation residues and transcription of the gene produces more than 10 alternative transcripts that are from 2075 to 2637 bp mRNA in size: isoform 1 (2637 bp), isoform 2 (2508 bp), isoform 3 (2376 bp), isoform 4 (2333 bp), isoform 5 (2412 bp), isoform 6 (2289 bp), isoform 7 (2283 bp), isoform 8 (2210) bp, isoform 9 (2165bp), and isoform 10 (2075 bp). Isoforms 9 and 10 are ubiquitous in expression. Isoform 8 is expressed specifically in skeletal muscle. Isoforms 1-7 are expressed predominantly in the central nervous system. An aberrant isoform has been reported to be expressed specifically in tumor cells. |
| Pseudogene | None reported. |
| Protein |
 | |
| At least 10 alternate protein isoforms of Bin1 are expressed in different tissues. Isoforms 9 and 10 are ubiquitous. Isoform 8 is muscle-specific. Isoforms 1-7 are expressed predominantly in the central nervous system. Two tumor-specific isoforms include an exon termed 12A that is normally spliced into Bin1 mRNA only with other exons expressed in the central nervous system. These tumor-specific isoforms occur commonly in cancer and they represent loss of function with regard to tumor suppression activity and nuclear localization capability. BAR, BAR domain; SH3, SH3 domain; MBD, Myc binding domain; CLAP, clathrin-associated protein binding region; PI, phosphoinositide binding region. Exons are numbered by reference to Wechsler-Reya et al. (1997). | |
| Description | Bin1 contains N-terminal BAR (Bin1/Amphihysin/Rvs) domain with predicted coiled-coil structure and a C-terminal SH3 domain. Bin1 encodes proteins of 409 to 593 amino acids; isoform 1 (593 aa), isoform 2 (550 aa), isoform 3 (506 aa), isoform 4 (497 aa), isoform 5 (518 aa), isoform 6 (482 aa), isoform 7 (475 aa), isoform 8 (454 aa), isoform 9 (439 aa), and isoform 10 (409 aa). Isoform 10 is the smallest and isoform 1 is the largest in size. Also, Bin1 has predicted molecular weight of 45432 to 64568 Da; isoform 1 (64568 Da), isoform 2 (59806 Da), isoform 3 (55044 Da), isoform 4 (54817 Da), isoform 5 (56368 Da), isoform 6 (52889 Da), isoform 7 (51606 Da), isoform 8 (50054 Da), isoform 9 (48127 Da), and isoform 10 (45432 Da). Isoforms 9 and 10 are ubiquitous in expression. Isoform 8 is expressed specifically in skeletal muscle. Isoforms 1-7 are expressed predominantly in the central nervous system. These 10 different splice isoforms differ widely in subcellular localization, tissue distribution, and ascribed functions, with isoforms 1-7 predominantly cytosolic but isoforms 8-10 found in both the nucleus and/or cytosol of certain cell types. |
| Expression | Bin1 is widely expressed. Patterns of isoform expression are noted above in the Diagram Legend. |
| Localisation | Bin1 is localized both in nuclear and cytosolic in the cerebral cortex and cerebellum of brain. Bin1 is localized mainly in nuclear in bone marrow cells whereas it is localized mainly in cytosolic in peripheral lymphoid cells. Bin1 is nuclear or nucleocytosolic in basal cells of skin, breast, or prostate, whereas it is cytosolic or plasma membrane localized in gastrointestinal cells. |
| Function | Bin1 encodes members of the BAR (Bin/Amphiphysin/Rvs) adapter family which have been implicated in membrane dynamics, such as vesicle fusion and trafficking, specialized membrane organization, actin organization, cell polarity, stress signaling, transcription, and tumor suppression. BAR adapter proteins are now recognized to be part of a larger superfamily of structurally related proteins that includes the so-called F-BAR and I-BAR adapter proteins. Membrane binding and tubulation: The Bin1 BAR domain can mediate binding and tubulation of curved membranes. Crystal structures of the BAR domains from human BIN1 and its fruit fly homolog reveal a dimeric banana-shaped 6-alpha-helix bundle that can nestle against the charged head groups on a curved lipid bilayer. Structural studies implicate specific alpha-helices in tubulation activity. Biochemical analyses implicate Bin1 in vesicle fission and fusion processes, with the SH3 domain providing an essential contribution to these processes through the recruitment of dynamins. Vesicle trafficking: Bin1 is implicated in endocytosis and intracellular endosome traffic through interactions with Rab5 guanine nucleotide exchange factors (Rab GEFs) and the sorting nexin protein Snx4. Complexes of neuronal Amph-I with neuron-specific isoforms of Bin1 (Amph-II) have been implicated in synaptic vesicle recycling in the brain. Genetic studies of the Bin1 homolog in budding yeast indicate an essential role in endocytosis, however, this role appears to be non-essential for homologs in fission yeast, fruit flies, and mice. Cell polarity: Genetic analyses of the Bin1 homologs in yeast and fruit flies suggest a integrative function in cell polarity, possibly mediated by effects on actin organization and vesicle trafficking. In budding yeast, the Bin1 homolog RVS167 lies at a central nodal point for integrating cell polarity signaling. Genetic ablation of the Bin1 homolog in fruit flies causes mislocalization of the cell polarity complex Dlg/Scr/Lgl, normally localized to the tight junction, that is implicated in epithelial polarity and suppression of tumor-like growths in flies. Transcription: Ubiquitous and muscle-specific isoforms of Bin1 that can localize to the nucleus can bind to c-Myc and suppress its transcriptional transactivation activity. Tethering the BAR domain of Bin1 to DNA is sufficient to repress transcription. Genetic studies in fission yeast demonstrate that the functional homolog hob1+ is essential to silence transcription of heterochromatin at telomeric and centromeric chromosomal loci by supporting a Rad6-Set1 pathway of transcriptional repression. Muscle function: Mutations of the human BIN1 gene are associated with centronuclear myopathy, a disorder marked by severe muscle weakness. Mouse genetic studies indicate that Bin1 is required for cardiac development. In skeletal muscle, Bin1 localizes to T tubules where it appears to support ion flux. In vitro studies of terminal muscle differentiation implicate Bin1 in myoblast cell cycle arrest and fusion during tubule formation. Apoptosis and Senescence: Bin1 is crucial for the function of default pathways of classical apoptosis or senescence triggered by the Myc or Raf oncogenes in primary cells. In human tumor cells, enforced expression of Bin1 triggers a non-classical program of cell death that is caspase independent and associated with activation of serine proteases. Tumor suppression: Attenuation of Bin1 function by silencing or missplicing is a frequent event in multiple human cancers including breast, prostate, skin, lung, and colon cancers. In breast cancer, attenuated expression of Bin1 is associated with increased metastasis and poor clinical outcome. In human tumor cells, ectopic expression of ubiquitous or muscle Bin1 isoforms causes growth arrest or caspase-independent cell death. A Bin1 missplicing event that occurs frequently in human cancers is sufficient to extinguish these activities. In primary rodent cells, Bin1 inhibits oncogenic co-transformation by Myc, adenovirus E1A, or mutant p53 but not SV40 T antigen. Mouse genetic studies establish that loss of Bin1 causes lung and liver cancers during aging. In mice where breast or colon tumors are initiated by carcinogen treatment, Bin1 deletion causes progression to more aggressive malignant states. Oncogenically transformed cells lacking Bin1 exhibit reduced susceptibility to apoptosis and increased proliferation, invasion, immune escape, and tumor formation. Activation of metalloproteinase MMP9 and immunosuppressive enzyme indoleamine 2,3-dioxygenase (IDO) have been implicated respectively in invasion and immune escape caused by Bin1 loss. Null phenotype in mouse: Bin1 knockout mice are perinatal lethal owing to myocardial hypertrophy where myofibrils of ventricular cardiomyocytes are severely disorganized. Genetic mosaic mice display increased susceptibility to inflammation, premalignant lesions in prostate and pancreas, and formation of liver and lung carcinoma. Female mosaic mice exhibit increased fecundity during aging. Tissue-specific gene ablation in skin or breast facilitates carcinogenesis. |
| Homology | The longest Bin1 alternate splice variant in human brain exhibits 71% amino acid sequences similarity and 55% amino acid sequence identity with amphiphysin-I (amph-I). Bin1 is also closely related to the mammalian amphiphysin-like genes Bin2 and Bin3. Genetic homologs of Bin1 that exist in budding and fission yeast (RVS167 and hob1+) and in fruit flies (amphiphysin) are well-characterized. |
| Mutations |
| Epigenetics | Attentuated expression or missplicing occurs in many cases of breast, prostate, lung, skin, brain and colon cancers. Expression analyses have identified Bin1 missplicing as among the most common missplicing events occurring in cancer. |
| Germinal | Germ-line mutations leading to nonsynonymous alterations in Bin1 have been associated with the familial muscle weakness disorder centronuclear myopathy, a disorder characterized by abnormal centralization of nuclei in muscle fibers. Two missense alterations the BAR domain that have been identified as loss of function mutations for membrane binding are K35N and D151N. Another mutation that has been identified, K575X, generates a prematurely terminated Bin1 protein implicated in loss of function. |
| Somatic | Loss of heterozygosity of Bin1 in cases of metastatic prostate cancer has been reported in the absence of mutation of the remaining allele. Infrequent instances of gene deletions have been reported in breast tumor cell lines. |
| Implicated in |
| Entity | Centronuclear myopathy |
| Note | Germ-line mutations of Bin1 are associated with formation of this rare familial disorder characterized by abnormal centralization of nuclei in muscle fibers and severe muscle weakness. In five affected individuals studied from three non-sanguineous families, two mutations extinguishing the membrane binding activity of the BAR domain were identified along one mutation causing a prematurely terminated Bin1 polypeptide. |
| Entity | Cardiomyopathy |
| Note | Dilated cardiomyopathy (DCM) is a leading cause of heart failure with as much as >25% of cases of familial etiology. A whole genome screen performed in a three-generation family with 12 affected individuals with autosomal dominant familial DCM defined linkage to chromosome 2q14-q22 where the human BIN1 gene is located. While BIN1 was not specifically identified as the germane locus, mouse studies indicate that genetic ablation causes cardiomyopathy during development. Moreover, in mice where Bin1 is ablated after birth in a tissue-specific manner in cardiomyocytes, a progressive cardiomyopathy develops consistent with the possibility that Bin1 loss of function may be a cause of DCM. |
| Entity | Breast Cancer |
| Oncogenesis | Breast cancer is the second leading cause of cancer death in women following lung cancer. Bin1 expression is attenuated significantly in >50% of cases of malignant breast cancer by immunohistochemical or RT-PCR analysis. Reduced levels of Bin1 are correlated to increased nodal metastasis and reduced survival in low or middle grade carcinomas. Mouse genetic studies indicate that Bin1 is non-essential for mammary gland development but that it is needed for the rapid kinetics of ductolobular remodeling during pregnancy and weaning. In mammary gland tumors initiated by the ras-activating carcinogen 7,12-dimethylbenzanthracene (DMBA), Bin1 loss strongly accentuates the formation of poorly differentiated tumors characterized by low tubule formation, high mitotic indices, and high degree of nuclear pleomorphism. Bin1 loss facilitates tumor progression at several intrinsic levels, including increased proliferation, survival, and motility of mouse mammary epithelial cells (MMECs) established from DMBA-induced tumors. |
| Entity | Lung Cancer |
| Oncogenesis | Lung cancer is a leading cause of death from cancer. Bin1 expression has been reported to be attenuated significantly in cases of lung adenocarcinoma by immunohistochemical analysis. Mouse genetic studies demonstrate that Bin1 loss is associated with formation of lung adenocarcinoma during aging, indicating that Bin1 attenuation drives disease incidence. |
| Entity | Colon Cancer |
| Oncogenesis | Colorectal cancer is the third most common cancer in the developed world. Bin1 expression has been reported to be attenuated significantly in ~50% of cases of colon cancer by Immunohistochemical analysis. Mouse genetic studies indicate that, in colon tumors initiated by treatment with the carcinogen dimethylhydrazine (DMH), Bin1 loss facilitates progression to more aggressive tumors with a higher multiplicity. |
| Entity | Skin Cancer |
| Oncogenesis | Skin cancer is the most common form of cancer. Basal cell cancer and squamous cell cancer are most common and treatable whereas melanoma is less common and deadlier. Studies of human melanoma revealed that Bin1 is inappropriately expressed as tumor cell-specific isoforms that include exon 12A, which is alternately spliced into isoforms found in the central nervous system but not normally on its own in melanocytes or other non-neuronal cells. This aberrant splicing event abolishes the tumor suppressor functions of Bin1 based on the loss of its anti-oncogenic and programmed cell death inducing activities in oncogenically transformed cells and melanoma cells. Mouse genetic studies indicate that Bin1 loss facilitates skin carcinogenesis. |
| Entity | Prostate Cancer |
| Oncogenesis | Prostate cancer is the leading cause of death in men older than 55 years of age. Loss of heterozygosity of the human BIN1 gene has been reported in ~40% of cases of metastatic prostate cancer. Bin1 is expressed in most primary tumors, even at slightly elevated levels relative to benign tissues, but it is frequently grossly attenuated in expression or inactivated by aberrant splicing in metastatic tumors and androgen-independent tumor cell lines. Ectopic expression suppresses the growth of prostate cancer cell lines in vitro. Mouse genetic studies indicate that Bin1 loss is associated with an increased incidence of prostate inflammation, atrophy, hypertrophy, and intraepithelial neoplasia during aging. |
| Entity | Neuroblastoma |
| Oncogenesis | Neuroblastoma (NB) is the most common solid tumor of childhood and is responsible for 15% of childhood cancer-related deaths. Bin1 expression is grossly reduced in MYCN amplified and metastatic NB compared with MYCN single-copy and localized NB as evaluated by real-time RT-PCR. Enforced expression of Bin1 in MYCN amplified human NB cell lines markedly inhibits colony formation. |
| Entity | Chronic Inflammation |
| Note | Mouse genetic studies indicate that Bin1 loss increases the general incidence of chronic inflammation in the heart, pancreas, liver, and prostate. |
| Entity | Female Fecundity |
| Note | Mouse genetic studies indicate that mosaic loss of Bin1 increases reproductive physiology during aging. Specifically, female mosaic mice exhibit extended fecundity during aging, retaining reproductive capability ~6 months longer than control mice. |
| Breakpoints |
| Note | None reported. |
| To be noted |
| N/A |
| External links |
| Bibliography |
| Genetic alterations in untreated metastases and androgen-independent prostate cancer detected by comparative genomic hybridization and allelotyping. |
| Cher ML, Bova GS, Moore DH, Small EJ, Carroll PR, Pin SS, Epstein JI, Isaacs WB, Jensen RH. |
| Cancer Res. 1996; 56(13): 3091-102. |
| PMID 8674067 |
| BIN1 is a novel MYC-interacting protein with features of a tumor suppressor. |
| Sakamuro D, Elliott K, Wechsler-Reya R, Prendergast GC. |
| Nature Genet. 1996; 14(1): 69-77. |
| PMID 8782822 |
| Amphiphysin II (SH3P9; BIN1), a member of the amphiphysin/RVS family, is concentrated in the cortical cytomatrix of axon initial segments and nodes of Ravier in brain and around T tubules in skeletal muscle. |
| Butler MH, David C, Ochoa GC, Freyberg Z, Daniell L, Grabs D, Cremona O, De Camilli P. |
| J Cell Biol. 1997; 137(6): 1355-67. |
| PMID 9182667 |
| Structural analysis of the human BIN1 gene: evidence for tissue-specific transcriptional regulation and alternate RNA splicing. |
| Wechsler-Reya R, Sakamuro D, Zhang J, Duhadaway J, Prendergast GC. |
| J Biol Chem. 1997; 272(50): 31453-8. |
| PMID 9395479 |
| A role for the putative tumor suppressor Bin1 in muscle cell differentiation. |
| Wechsler-Reya R , Elliott KJ, Prendergast GC. |
| Mol Cell Biol. 1998; 18(1): 566-75. |
| PMID 9418903 |
| Mechanism for elimination of a tumor suppressor: aberrant splicing of a brain-specific exon causes loss of function of Bin1 in melanoma. |
| Ge K, DuHadaway J, Du W, Herlyn M, Rodeck U, Prendergast GC. |
| Proc Natl Acad Sci U S A. 1999; 96(17):9689-94. |
| PMID 10449755 |
| Investigation of a family with autosomal dominant dilated cardiomyopathy defines a novel locus on chromosome 2q14-q22. |
| Jung M, Poepping I, Perrot A, Ellmer AE, Wienker TF, Dietz R, Reis A, Osterziel KJ. |
| Am J Hum Genet. 1999; 65(4): 1068-77. |
| PMID 10486326 |
| Losses of the tumor suppressor Bin1 in breast carcinoma are frequent and reflect deficits in a programmed cell death capacity. |
| Ge K, DuHadaway J, Sakamuro D, Wechsler-Reya R, Reynolds C, Prendergast GC. |
| Int J Cancer. 2000; 85(3) 376-83. |
| PMID 10652430 |
| Loss of heterozygosity and tumor suppressor activity of Bin1 in prostate carcinoma. |
| Ge K, Minhas F, Duhadaway J, Mao NC, Wilson D, Buccafusca R, Sakamuro D, Nelson P, Malkowicz SB, Tomaszewski J, Prendergast GC. |
| Int J Cancer. 2000; 86(2): 155-61. |
| PMID 10738240 |
| BIN1 inhibits colony formation and induces apoptosis in neuroblastoma cell lines with MYCN amplification. |
| Hogarty MD, Liu X, Thompson PM, White PS, Sulman EP, Maris JM, Brodeur GM. |
| Med Pediatr Oncol. 2000; 35(6): 559-62. |
| PMID 11107117 |
| Amphiphysin is necessary for organization of the excitation-contraction coupling machinery of muscles, but not for synaptic vesicle endocytosis in Drosophila. |
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| Genes Dev. 2001; 15(22): 2967-79. |
| PMID 11711432 |
| Drosophila Amphiphysin is implicated in protein localization and membrane morphogenesis but not in synaptic vesicle endocytosis. |
| Zelhof AC, Bao H, Hardy RW, Razzaq A, Zhang B, Doe CQ. |
| Development. 2001; 128(24): 5005-15. |
| PMID 11748137 |
| Amphiphysin 2 (Bin1) and T-tubule biogenesis in muscle. |
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| PMID 12183633 |
| Transformation-selective apoptotic program triggered by farnesyltransferase inhibitors requires Bin1. |
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| PMID 12789266 |
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| DuHadaway JB, Lynch FJ, Brisbay S, Bueso-Ramos C, Troncoso P, McDonnell T, Prendergast GC. |
| J Cell Biochem. 2003; 88(3):635-42. |
| PMID 12532338 |
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| J Cell Sci. 2003; 116(Pt 10): 1937-48. |
| PMID 12668730 |
| Targeted disruption of the murine Bin1/Amphiphysin II gene does not disable endocytosis but results in embryonic cardiomyopathy with aberrant myofibril formation. |
| Muller AJ, Baker JF, DuHadaway JB, Ge K, Farmer G, Donover PS, Meade R, Reid C, Grzanna R, Roach AH, Shah N, Soler AP, Prendergast GC |
| Mol Cell Biol. 2003; 23(12): 4295-306. |
| PMID 12773571 |
| Expression of a MYCN-interacting isoform of the tumor suppressor BIN1 is reduced in neuroblastomas with unfavorable biological features. |
| Tajiri T, Liu X, Thompson PM, Tanaka S, Suita S, Zhao H, Maris JM, Prendergast GC, Hogarty MD. |
| Clin Cancer Res. 2003; 9(9): 3345-3355. |
| PMID 12960121 |
| Regulation of Bin1 SH3 domain binding by phosphoinositides. |
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| PMID 15483625 |
| Targeted deletion of the suppressor gene Bin1/Amphiphysin2 enhances the malignant character of transformed cells. |
| Muller AJ, DuHadaway JB, Donover PS, Sutanto-Ward E, Prendergast GC. |
| Cancer Biol. Ther. 2004; 3(12): 1236-42. |
| PMID 15611650 |
| A structure-based model of the c-Myc/Bin1 protein interaction shows alternative splicing of Bin1 and c-Myc phosphorylation are key binding determinants. |
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| PMID 15992821 |
| The crystal structure of the BAR domain from human Bin1/amphiphysin II and it implications for molecular recognition. |
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| PMID 17059209 |
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| PMID 16949824 |
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| Ren G, Vajjhala P, Lee JS, Winsor B, Munn AL. |
| Microbiol Mol Biol Rev. 2006;70(1):37-120. (REVIEW) |
| PMID 16524918 |
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| PMID 16516635 |
| Bin1 ablation increases susceptibility to cancer during aging, particularly lung cancer. |
| Chang MY, Boulden J, Katz JB, Wang L, Meyer TJ, Soler AP, Muller AJ, Prendergast GC. |
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| PMID 17699764 |
| Bin1 ablation in mammary gland delays tissue remodeling and drives cancer progression. |
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| PMID 17210688 |
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| Chitu V, Stanley ER. |
| Trends Cell Biol. 2007; 17(3): 145-56 |
| PMID 17296299 |
| Bin1 attenuation in breast cancer is correlated to nodal metastasis and reduced survival. |
| Ghaneie A, Zemba-Palko V, Itoh H, Itoh K, Sakamuro D, Nakamura S, Soler AP, Prendergast GC. |
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| PMID 17218774 |
| Mutations in amphiphysin 2 (BIN1) disrupt interaction with dynamin 2 and cause autosomal recessive centronuclear myopathy. |
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| PMID 17676042 |
| Bin1 interacts with and restrains the DNA end-binding protein complex Ku. |
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| Cell Cycle. 2007; 6(15): 1914-8. |
| PMID 17671430 |
| Bin1 homolog hob1 supports a Rad6-Set1 pathway of transcriptional repression in fission yeast. |
| Ramalingam A, Prendergast GC. |
| Cell Cycle. 2007; 6(13): 1655-62. |
| PMID 17611416 |
| Adenovirus E1A oncoprotein liberates c-Myc activity to promote cell proliferation through abating Bin1 expression via an Rb/E2F1-dependent mechanism. |
| Kinney EL, Tanida S, Rodrigue AA, Johnson JK, Tompkins VS, Sakamuro D. |
| J Cell Physiol. 2008; 216(3): 621-31. |
| PMID 18348166 |
| Oncogenic BRAF induces senescence and apoptosis through pathways mediated by the secreted protein IGFBP7. |
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| PMID 18267069 |
| REVIEW articles | automatic search in PubMed |
| Last year publications | automatic search in PubMed |
| Contributor(s) |
| Written | 09-2008 | Mee Young Chang, George C Prendergast |
| Lankenau Institute for Medical Research, Lankenau Hospital, Wynnewood, Pennsylvania 19096, USA |
| Citation |
| This paper should be referenced as such : |
| Chang MY, Prendergast GC . BIN1 (bridging integrator 1). Atlas Genet Cytogenet Oncol Haematol. September 2008 . |
| URL : http://AtlasGeneticsOncology.org/Genes/BIN1ID794ch2q14.html |
The various updated versions of this paper are referenced and archived by INIST as such : |
| http://documents.irevues.inist.fr/bitstream/2042/44530/1/09-2008-BIN1ID794ch2q14.pdf [ Bibliographic record ] |
| © Atlas of Genetics and Cytogenetics in Oncology and Haematology | indexed on : Thu Feb 6 12:54:35 CET 2014 |
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