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Human Polyclonal KHDRBS1 Primary Antibody pour ICC, IF - ABIN4351941
Lawrence, Schafer, Rieder: The nuclear protein Sam68 is cleaved by the FMDV 3C protease redistributing Sam68 to the cytoplasm during FMDV infection of host cells. dans Virology 2012
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Results revealed that upregulation of Sam68 significantly inhibited cisplatin-induced apoptosis in oral tongue squamous cell carcinoma cells.
The PRMT2 (Montrer PRMT2 Anticorps) interacts with SAM68 in cells and regulates its subcellular localization via the SH3 domain (Montrer ITSN1 Anticorps) of PRMT2 (Montrer PRMT2 Anticorps), prompting us to investigate the potential role of PRMT2 (Montrer PRMT2 Anticorps) in BCL-X (Montrer BCL2L1 Anticorps) alternative splicing.
Data suggest that the first 22 bp of exon 3 in BIRC5 (Montrer BIRC5 Anticorps) contain cis (Montrer CISH Anticorps)-acting elements that enhance the exclusion of exon 3 to generate the survivin (Montrer BIRC5 Anticorps) DEx3 mRNA isoform via exclusion/deletion of exon 3; Sam68 is a possible trans-acting factor that binds to this cis (Montrer CISH Anticorps)-acting element and regulates exon 3 splicing. (BIRC5/survivin (Montrer BIRC5 Anticorps) = baculoviral IAP repeat containing 5 (Montrer BIRC5 Anticorps); Sam68 = GAP-associated tyrosine phosphoprotein p62)
our results indicated that Sam68 modulates apoptosis of intestinal epithelial cells via mediating NF-kappaB (Montrer NFKB1 Anticorps) activation in ulcerative colitis
Sam68 possibly participated in the progresses of T-acute lymphoblastic leukemia at least partially via AKT (Montrer AKT1 Anticorps)/mTOR (Montrer FRAP1 Anticorps) signaling pathway
Sam68 is essential for DNA damage-induced NF-kappaB (Montrer NFKB1 Anticorps) activation and colon tumorigenesis.
These findings define a hitherto novel mechanism of action for Sam68 in governing p53 (Montrer TP53 Anticorps) transcriptional activation, and represent the first report of Sam68 in the regulation of tumor suppressor activities.
HNRNPL (Montrer HNRNPL Anticorps) acts as the adaptor to combine the two substructures and form the intact Sam68 nuclear body through the interaction of two sets of RNA recognition motifs with the putative architectural RNA in the respective substructures.
Sam68 was overexpressed in EOC tissue in association with such cancer malignant factors of FIGO stage, histological grade, and lymph node metastasis, and also positively regulated the proliferation of EOC cells.
Taken together, these results illuminated that enterovirus 71 infections can induce stress granule formation, and Sam68, as a stress granule component, migrates alone with stress granules dependent on intact microtubule upon the viral infections.
Sam68-haploinsufficiency significantly delayed the onset of tumors in mice lacking p53 (Montrer TP53 Anticorps) and prolonged their survival, indicating that Sam68 accelerates the development of p53 (Montrer TP53 Anticorps)-deficient tumors.
Sam68 deletion diminishes gamma-irradiation-triggered PAR (Montrer AFG3L2 Anticorps) synthesis and NF-kappaB (Montrer NFKB1 Anticorps) activation in colon epithelial cells (CECs), thus hampering the expression of anti-apoptotic molecules in situ and facilitating CECs to undergo apoptosis in mice post whole-body gamma-irradiation (WBIR).
This study identifies Sam68 as a key regulator of neural progenitor cell self-renewal and establishes a novel link between modulation of ALDH1A3 (Montrer ALDH1A3 Anticorps) expression and maintenance of high glycolytic metabolism in the developing cortex.
Sam68 may function as an immune rheostat that balances the activation of NF-kappaB (Montrer NFKB1 Anticorps) p65 (Montrer NFkBP65 Anticorps) and c-Rel (Montrer NFkBP65 Anticorps), as well as MAPK (Montrer MAPK1 Anticorps), revealing a potential novel target to manipulate TLR signaling.
Sam68 plays a crucial role in DNA damage response via regulating DNA damage-initiated PAR (Montrer AFG3L2 Anticorps) production.
Sam68 and T-STAR (Montrer KHDRBS3 Anticorps) could regulate alternative splicing of some pre-mRNAs by bringing two distant UAA motifs into proximity and looping out regions of the pre-mRNA.
SAM68 is a physiological regulator of SMN2 (Montrer SMN1 Anticorps) splicing in a spinal muscular atrophy mouse model.
Data (including data from knockout mice) suggest expression of Sam68 plays role in adipogenesis of white adipose tissue versus brown adipose tissue; Sam68 appears to regulate adiposity and energy homeostasis (balance of energy intake/expenditure).
This gene encodes a member of the K homology domain-containing, RNA-binding, signal transduction-associated protein family. The encoded protein appears to have many functions and may be involved in a variety of cellular processes, including alternative splicing, cell cycle regulation, RNA 3'-end formation, tumorigenesis, and regulation of human immunodeficiency virus gene expression. Alternative splicing results in multiple transcript variants.
GAP-associated tyrosine phosphoprotein p62 (Sam68)
, KH domain-containing, RNA-binding, signal transduction-associated protein 1
, p21 Ras GTPase-activating protein-associated p62
, src-associated in mitosis 68 kDa protein
, GAP-associated phosphoprotein p62
, KH domain containing, RNA binding, signal transduction associated 1
, GAP-associated tyrosine phosphoprotein p62
, src associated in mitosis, 68 kDa
, KH domain RNA-binding protein Sam68