Mechanism for elimination of a tumor suppressor: aberrant splicing of a brain-specific exon causes loss of function of Bin1 in melanoma. - Test2 - elhamkhani - TriplyDB

Mechanism for elimination of a tumor suppressor: aberrant splicing of a brain-specific exon causes loss of function of Bin1 in melanoma.

Mechanism for elimination of a tumor suppressor: aberrant splicing of a brain-specific exon causes loss of function of Bin1 in melanoma.

http://www.wikidata.org/entity/Q36429965

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Human BIN3 complements the F-actin localization defects caused by loss of Hob3p, the fission yeast homolog of Rvs161p Transcription coactivator TRAP220 is required for PPAR gamma 2-stimulated adipogenesis The BAR domain proteins: molding membranes in fission, fusion, and phagy TLS-ERG leukemia fusion protein inhibits RNA splicing mediated by serine-arginine proteins Underediting of glutamate receptor GluR-B mRNA in malignant gliomas The pathobiology of splicing Discovery of novel splice forms and functional analysis of cancer-specific alternative splicing in human expressed sequences Evidence that public database records for many cancer-associated genes reflect a splice form found in tumors and lack normal splice forms.Splicing Regulators and Their Roles in Cancer Biology and Therapy Trial watch: IDO inhibitors in cancer therapy Late-Onset Alzheimer's Disease Genes and the Potentially Implicated Pathways Defective control of pre-messenger RNA splicing in human disease Tandem arrangement of the clathrin and AP-2 binding domains in amphiphysin 1 and disruption of clathrin coat function by amphiphysin fragments comprising these sites Mutations in amphiphysin 2 (BIN1) disrupt interaction with dynamin 2 and cause autosomal recessive centronuclear myopathy Histone methylation regulator PTIP is required for PPARgamma and C/EBPalpha expression and adipogenesis Alternative splice variants in TIM barrel proteins from human genome correlate with the structural and evolutionary modularity of this versatile protein fold Hepatitis C virus NS5A is able to competitively displace c-Myc from the Bin1 SH3 domain in vitro.Bin1 SRC homology 3 domain acts as a scaffold for myofiber sarcomere assembly Early Carcinogenesis Involves the Establishment of Immune Privilege via Intrinsic and Extrinsic Regulation of Indoleamine 2,3-dioxygenase-1: Translational Implications in Cancer Immunotherapy.Libraries enriched for alternatively spliced exons reveal splicing patterns in melanocytes and melanomas.Regulation of Cardiomyocyte T-Tubular Structure: Opportunities for Therapy.Cardiac BIN1 folds T-tubule membrane, controlling ion flux and limiting arrhythmia.BAR the door: cancer suppression by amphiphysin-like genes MicroRNA (miRNA)-mediated interaction between leukemia/lymphoma-related factor (LRF) and alternative splicing factor/splicing factor 2 (ASF/SF2) affects mouse embryonic fibroblast senescence and apoptosis WWOX mRNA expression profile in epithelial ovarian cancer supports the role of WWOX variant 1 as a tumour suppressor, although the role of variant 4 remains unclear.Inhibition of indoleamine 2,3-dioxygenase, an immunoregulatory target of the cancer suppression gene Bin1, potentiates cancer chemotherapy.Indoleamine 2,3-dioxygenase pathways of pathogenic inflammation and immune escape in cancer Placenta-specific novel splice variants of Rho GDP dissociation inhibitor β are highly expressed in cancerous cells.Cardiac T-Tubule Microanatomy and Function.Regulation of E2F1-induced apoptosis by poly(ADP-ribosyl)ation The RNA-binding protein QKI suppresses cancer-associated aberrant splicing.Identification of a novel effector domain of BIN1 for cancer suppression.Identification of a human TFPI-2 splice variant that is upregulated in human tumor tissues.The splicing factor SRSF1 regulates apoptosis and proliferation to promote mammary epithelial cell transformation.Characterization of bridging integrator 1 (BIN1) as a potential tumor suppressor and prognostic marker in hepatocellular carcinoma The gene encoding the splicing factor SF2/ASF is a proto-oncogene Indoleamine 2,3-dioxygenase in cancer: targeting pathological immune tolerance with small-molecule inhibitors.BIN1 regulates dynamic t-tubule membrane.Whole genome exon arrays identify differential expression of alternatively spliced, cancer-related genes in lung cancer.A phase I study of indoximod in patients with advanced malignancies

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Mechanism for elimination of a tumor suppressor: aberrant splicing of a brain-specific exon causes loss of function of Bin1 in melanoma.

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P2860

Amphiphysin II (SH3P9; BIN1), a member of the amphiphysin/Rvs family, is concentrated in the cortical cytomatrix of axon initial segments and nodes of ranvier in brain and around T tubules in skeletal muscle

BIN1 is a novel MYC-interacting protein with features of a tumour suppressor

A role for the putative tumor suppressor Bin1 in muscle cell differentiation

Amphiphysin heterodimers: potential role in clathrin-mediated endocytosis

The murine Bin1 gene functions early in myogenesis and defines a new region of synteny between mouse chromosome 18 and human chromosome 2

Identification and characterization of a nerve terminal-enriched amphiphysin isoform

cDNA cloning of a novel amphiphysin isoform and tissue-specific expression of its multiple splice variants

Structural analysis of the human BIN1 gene. Evidence for tissue-specific transcriptional regulation and alternate RNA splicing

Multiple amphiphysin II splice variants display differential clathrin binding: identification of two distinct clathrin-binding sites

Bin1 functionally interacts with Myc and inhibits cell proliferation via multiple mechanisms.

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