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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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NCL and Sam68 could recognize their specific motifs and directly bind to EXON1 of CYTOR. Moreover, EXON1 was the key functional site mediating the interaction of CYTOR with NCL and Sam68. NCL and Sam68 functioned as oncogenes to promote colorectal cancer (CRC) progression. Further results confirmed that the heterotrimeric complex of CYTOR, NCL and Sam68 activated the NF-kappaB pathway and EMT to contribute to CRC progr...
Vimentin and Sam68, are identified as bona fide SRMS substrates through in vitro and in vivo assays.
Case Report: congenital CD34-positive dermohypodermal spindle-cell neoplasm occurring in a female infant and harboring a novel KHDRBS1-NTRK3 fusion.
findings suggested that Sam68 contributed to the production of inflammatory cytokines, proliferation, migration, and invasion of Rheumatoid Arthritis (RA) Fibroblast-like Synoviocytes (FLS( through the NF-kappaB P65 signal transduction pathway and underscored the importance of Sam68 in the inflammation process of RA.
Moreover, SRSF10, hnRNP A1/A2 and Sam68 collaborate to drive the DNA damage-induced splicing response of several transcripts that produce components implicated in apoptosis, cell-cycle control and DNA repair.
SAM68 is required for efficient recruitment of PUM2 to NORAD, regulation of Pum activity by NORAD, and proper chromosome segregation in mammalian cells.
Results revealed that upregulation of Sam68 significantly inhibited cisplatin-induced apoptosis in oral tongue squamous cell carcinoma cells.
The PRMT2 interacts with SAM68 in cells and regulates its subcellular localization via the SH3 domain of PRMT2, prompting us to investigate the potential role of PRMT2 in BCL-X alternative splicing.
Data suggest that the first 22 bp of exon 3 in BIRC5 contain cis-acting elements that enhance the exclusion of exon 3 to generate the survivin DEx3 mRNA isoform via exclusion/deletion of exon 3; Sam68 is a possible trans-acting factor that binds to this cis-acting element and regulates exon 3 splicing. (BIRC5/survivin = baculoviral IAP repeat containing 5; Sam68 = GAP-associated tyrosine phosphoprotein p62)
our results indicated that Sam68 modulates apoptosis of intestinal epithelial cells via mediating NF-kappaB activation in ulcerative colitis
Sam68 possibly participated in the progresses of T-acute lymphoblastic leukemia at least partially via AKT/mTOR signaling pathway
Sam68 is essential for DNA damage-induced NF-kappaB activation and colon tumorigenesis.
These findings define a hitherto novel mechanism of action for Sam68 in governing p53 transcriptional activation, and represent the first report of Sam68 in the regulation of tumor suppressor activities.
HNRNPL 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.
The host factor Sam68 interact with both, foot-and-mouth disease virus RNA motifs in the internal ribosome binding site and viral non-structural proteins 3C(pro) and 3D(pol).
Sam68 has separable effects on the regulation of AR-V7 expression and transcriptional activity, through its RNA-binding capacity.
The RNA-binding protein Sam68 regulates tumor cell viability and hepatic carcinogenesis by inhibiting the transcriptional activity of FOXOs
Sam68 Promotes NF-kappaB Activation and Apoptosis Signaling in Articular Chondrocytes during Osteoarthritis
Sam68-haploinsufficiency significantly delayed the onset of tumors in mice lacking p53 and prolonged their survival, indicating that Sam68 accelerates the development of p53-deficient tumors.
Sam68 deletion diminishes gamma-irradiation-triggered PAR synthesis and NF-kappaB 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 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 p65 and c-Rel, as well as MAPK, revealing a potential novel target to manipulate TLR signaling.
Sam68 plays a crucial role in DNA damage response via regulating DNA damage-initiated PAR production.
Sam68 and T-STAR 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 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).
Depletion of p31S6K1 with small interfering RNAs (siRNAs) partially restored adipogenesis of Sam68-deficient preadipocytes.
Emerging roles for Sam68 in adipogenesis and neuronal development.
Our research identifies a role for Sam68 in synaptodendritic posttranscriptional regulation of actb and may provide insight into the pathophysiology of fragile X tremor/ataxia syndrome
Results suggest a novel role for SAM68 in the miRNA pathway during spermatogenesis.
Sam68 regulates alternative splicing during adipogenesis.
We demonstrated that the FMDV 3C(pro) induced the cleavage of nuclear RNA-binding protein Sam68 C-terminus containing the nuclear localization sequence (NLS and stimulated the redistribution of Sam68 to the cytoplasm.
Findings uncover SAM68 as a key regulator of dynamic control of Nrxn1 molecular diversity and activity-dependent alternative splicing in the central nervous system.
These studies identify a new crucial function for Sam68 in the regulation of female fertility.
required for the correct progression of spermatogenesis
identified hnRNP L as a novel Sam68-interacting protein partner.
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