Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all species
Show all synonyms
Select your species
Silence of p62 promotes apoptosis induced by mitochondrial depolarization.
Rare variants in SQSTM1 (show SQSTM1 ELISA Kits) are risk for sporadic inclusion body myositis.
The PRMT2 (show PRMT2 ELISA Kits) interacts with SAM68 in cells and regulates its subcellular localization via the SH3 domain (show ITSN1 ELISA Kits) of PRMT2 (show PRMT2 ELISA Kits), prompting us to investigate the potential role of PRMT2 (show PRMT2 ELISA Kits) in BCL-X (show BCL2L1 ELISA Kits) alternative splicing.
The WDR81 (show WDR81 ELISA Kits) coordinates p62 (show GTF2H1 ELISA Kits) and LC3C to facilitate autophagic removal of Ub proteins, and provide important insights into CAMRQ2 (show WDR81 ELISA Kits) syndrome, a WDR81 (show WDR81 ELISA Kits)-related developmental disorder.
SQSTM1 (show SQSTM1 ELISA Kits)-Nup214 (show NUP214 ELISA Kits), although mostly cytoplasmic, also forms nuclear bodies and inhibits nuclear protein (show RDBP ELISA Kits) but not poly(A)(+) RNA export.
autophagy upregulation by Sequestosome 1 (p62 (show SQSTM1 ELISA Kits)/SQSM1) knockdown ameliorated this cell injury and relieved insulin (show INS ELISA Kits) resistance
This work suggests that UVA-induced p62 (show GTF2H1 ELISA Kits) acts through COX-2 (show COX2 ELISA Kits) to promote skin tumor growth and progression.
we provide evidence that p62 (show GTF2H1 ELISA Kits) is implicated in the activation of NF-kappaB (show NFKB1 ELISA Kits) signaling that is partly dependent on RIP1
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 phosphorylation of SQSTM1 (show SQSTM1 ELISA Kits) by AMP-activated protein kinase (AMPK (show PRKAA2 ELISA Kits)) and translocation of SQSTM1 (show SQSTM1 ELISA Kits) to mitochondria drives autophagic cell death in adult hippocampal neural stem cells; activation of AMPK (show PRKAA1 ELISA Kits) promotes autophagic cell death; inhibition of AMPK (show PRKAA1 ELISA Kits) (by enzyme inhibitor or RNA interference) suppresses autophagic cell death. (SQSTM1 (show SQSTM1 ELISA Kits) = sequestosome 1 (show SQSTM1 ELISA Kits))
our results indicated that Sam68 modulates apoptosis of intestinal epithelial cells via mediating NF-kappaB (show NFKB1 ELISA Kits) activation in ulcerative colitis
Sam68 may function as an immune rheostat that balances the activation of NF-kappaB (show NFKB1 ELISA Kits) p65 (show NFkBP65 ELISA Kits) and c-Rel (show NFkBP65 ELISA Kits), as well as MAPK (show MAPK1 ELISA Kits), 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 ELISA Kits) production.
Sam68 is essential for DNA damage-induced NF-kappaB (show NFKB1 ELISA Kits) 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 ELISA Kits) 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