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Human KHDRBS1 Protein expressed in Wheat germ - ABIN1308538
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. in Virology 2012
Silence of p62 promotes apoptosis induced by mitochondrial depolarization.
Rare variants in SQSTM1 (show SQSTM1 Proteins) are risk for sporadic inclusion body myositis.
The PRMT2 (show PRMT2 Proteins) interacts with SAM68 in cells and regulates its subcellular localization via the SH3 domain of PRMT2 (show PRMT2 Proteins), prompting us to investigate the potential role of PRMT2 (show PRMT2 Proteins) in BCL-X (show BCL2L1 Proteins) alternative splicing.
The WDR81 coordinates p62 and LC3C to facilitate autophagic removal of Ub proteins, and provide important insights into CAMRQ2 syndrome, a WDR81-related developmental disorder.
SQSTM1-Nup214, although mostly cytoplasmic, also forms nuclear bodies and inhibits nuclear protein but not poly(A)(+) RNA export.
autophagy upregulation by Sequestosome 1 (p62 (show SQSTM1 Proteins)/SQSM1) knockdown ameliorated this cell injury and relieved insulin (show INS Proteins) resistance
This work suggests that UVA-induced p62 (show GTF2H1 Proteins) acts through COX-2 to promote skin tumor growth and progression.
we provide evidence that p62 (show GTF2H1 Proteins) is implicated in the activation of NF-kappaB (show NFKB1 Proteins) signaling that is partly dependent on RIP1 (show UQCRFS1 Proteins)
In this study, we first observed that p62-positive intranuclear aggregates also appeared in controls and were not specific for the Neuronal Intranuclear Hyaline Inclusion Disease cases.
Data suggest that the first 22 bp of exon 3 in BIRC5 (show BIRC5 Proteins) contain cis (show CISH Proteins)-acting elements that enhance the exclusion of exon 3 to generate the survivin (show BIRC5 Proteins) DEx3 mRNA isoform via exclusion/deletion of exon 3; Sam68 is a possible trans-acting factor that binds to this cis (show CISH Proteins)-acting element and regulates exon 3 splicing. (BIRC5/survivin (show BIRC5 Proteins) = baculoviral IAP repeat containing 5 (show BIRC5 Proteins); Sam68 = GAP-associated tyrosine phosphoprotein p62)
our results indicated that Sam68 modulates apoptosis of intestinal epithelial cells via mediating NF-kappaB (show NFKB1 Proteins) activation in ulcerative colitis
Sam68 may function as an immune rheostat that balances the activation of NF-kappaB (show NFKB1 Proteins) p65 (show NFkBP65 Proteins) and c-Rel (show NFkBP65 Proteins), as well as MAPK (show MAPK1 Proteins), revealing a potential novel target to manipulate TLR signaling.
Sam68 plays a crucial role in DNA damage response via regulating DNA damage-initiated PAR (show AFG3L2 Proteins) production.
Sam68 is essential for DNA damage-induced NF-kappaB (show NFKB1 Proteins) activation and colon tumorigenesis.
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 (show SMN1 Proteins) 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
This gene encodes a multifunctional protein that binds ubiquitin and regulates activation of the nuclear factor kappa-B (NF-kB) signaling pathway. The protein functions as a scaffolding/adaptor protein in concert with TNF receptor-associated factor 6 to mediate activation of NF-kB in response to upstream signals. Alternatively spliced transcript variants encoding either the same or different isoforms have been identified for this gene. Mutations in this gene result in sporadic and familial Paget disease of bone.
GAP-associated phosphoprotein p62
, KH domain containing, RNA binding, signal transduction associated 1
, 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 tyrosine phosphoprotein p62
, src associated in mitosis, 68 kDa
, KH domain RNA-binding protein Sam68
, EBI3-associated protein of 60 kDa
, EBI3-associated protein p60
, oxidative stress induced like
, phosphotyrosine independent ligand for the Lck SH2 domain p62
, phosphotyrosine-independent ligand for the Lck SH2 domain of 62 kDa
, ubiquitin-binding protein p62