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Validated All-in-One™ qPCR Primer for PDCD4(NM_014456.4) Search again
Product ID:
HQP007623
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
H731
Gene Description:
programmed cell death 4
Target Gene Accession:
NM_014456.4(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.
Summary
This gene encodes a protein localized to the nucleus in proliferating cells. Expression of this gene is modulated by cytokines in natural killer and T cells. The gene product is thought to play a role in apoptosis but the specific role has not yet been determined. Two transcripts encoding different isoforms have been identified. [provided by RefSeq].
Gene References into function
- up-regulated in senescent diploid fibroblasts
- Results indicate that not only binding to eIF4A but also prevention of eIF4A binding to the MA-3 domain of eIF4Gc contributes to the mechanism by which Pdcd4 inhibits translation.
- overexpression of PDCD4 in carcinoid cells results in inhibition of cell proliferation.
- expression of pdcd4 as an indirect suppressor of CDK1/cdc2 is lost in progressed carcinomas of lung, breast, colon, and prostate
- Pdcd4 suppresses tumor progression in colon carcinoma cells by the novel mechanism of down-regulating MAP4K1 transcription, with consequent inhibition of c-Jun activation and AP-1-dependent transcription.
- data suggest that PDCD4 is a proapoptotic molecule involved in TGF-beta1-induced apoptosis in human HCC cells, and a possible tumor suppressor in hepatocarcinogenesis
- in response to mitogens, PDCD4 was rapidly phosphorylated by protein kinase S6K1 & then degraded by ubiquitin ligase SCF(betaTRCP); it is proposed that regulated degradation of PDCD4 in response to mitogens allows efficient protein synthesis & cell growt
- These data suggest Pdcd4 as a new negative regulator of intravasation, and qas the invasion-related gene u-PAR. It is the first study to implicate Pdcd4 regulation of gene expression via Sp1/Sp3.
- Downregulation of tumor suppressor Pdcd4 promotes colonic neoplastic transformation and tumor invasion
- Loss of programmed cell death 4 expression is associated with colorectal cancer
- we conclude that the function of Pdcd4 might be cell type specific. A role for Pdcd4 in apoptosis or as a tumor suppressor might be limited to certain cell types.
- Programmed Cell Death 4 (PDCD4) is regulated by microrna miR-21 and demonstrate that PDCD4 is a functionally important target for miR-21 in breast cancer cells.
- the PDCD4 MA3 domains compete with the eIF4G MA3 domain and RNA for eIF4A binding. PDCD4 inhibits translation initiation by displacing eIF4G and RNA from eIF4A.
- Pdcd4 is a translation inhibitor targeted for degradation during tumor promotion
- mir-21 functions as an oncogene by a mechanism that involves translational repression of the tumor suppressor Pdcd4
- results provide the first evidence that Pdcd4 is important role in the DNA-damage response and suggest that low levels of Pdcd4 expression observed in certain tumor cells contribute to tumorigenesis by affecting the fate of DNA-damaged cells
- in squamous cell carcinoma lung cancer lines, alterations in Pdcd4 mRNA and protein levels are not directly linked.
- Suppression of Pdcd4 resulted in an increased release of CgA and Sg II and was accompanied by an up-regulation of intracellular PC1.
- Inhibition of miR-21 increases endogenous levels of PDCD4 in cell line T98G and over-expression miR-21 inhibits PDCD4-dependent apoptosis
- Lost or reduced PDCD4 expression is associated with the progression of ovarian serous cystadenocarcinomas and may serve as an important prognostic marker.
- Structural and mutational analyses reveal that Pdcd4 inhibits translation initiation by trapping eIF4A in an inactive conformation, and blocking its incorporation into the eIF4F complex.