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Validated All-in-One™ qPCR Primer for KHSRP(NM_003685.2) Search again
Product ID:
HQP021301
(click here to view gene annotation page)
Species:
Human
Symbol:
Alias:
FBP2, FUBP2, KSRP, p75
Gene Description:
KH-type splicing regulatory protein
Target Gene Accession:
NM_003685.2(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Gene References into function
- KSRP do indeed interact with the c-src transcript in vivo, and that these associations change with the differentiated state of the cell.
- KSRP, a KH domain-containing ARE-BP, is an essential factor for ARE-directed mRNA decay. Some KH motifs of KSRP mediate RNA binding, mRNA decay, and interactions with the exosome.
- IL-8 RNA from IL-1beta-stimulated cytoplasmic extract revealed a 20-fold greater association of transcript with the stabilizing factor HuR vs. the destabilizing factor KSRP in breast cancer cells
- KHSRP, tethered to mRNAs, elicits mRNA decay.
- propose KSRP phosphorylation as a link between phosphatidylinositol 3-kinase-AKT signaling and beta-catenin accumulation
- These results indicate that KSRP functions as a limiting factor in inflammatory gene expression.
- These data indicate a novel role for KSRP in parathyroid hormone gene expression.
- The over-expression of a novel protein family, far upstream binding proteins (FUBPs) was identified in both stages of hepatocellular carcinoma and confirmed by western blots.
- The authors report that phosphorylation leads to the unfolding of the structurally atypical and unstable KH1, creating a site for 14-3-3zeta binding.
