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Validated All-in-One™ qPCR Primer for DUSP3(NM_004090.3) Search again
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:
Summary
The protein encoded by this gene is a member of the dual specificity protein phosphatase subfamily. These phosphatases inactivate their target kinases by dephosphorylating both the phosphoserine/threonine and phosphotyrosine residues. They negatively regulate members of the mitogen-activated protein (MAP) kinase superfamily (MAPK/ERK, SAPK/JNK, p38), which are associated with cellular proliferation and differentiation. Different members of the family of dual specificity phosphatases show distinct substrate specificities for various MAP kinases, different tissue distribution and subcellular localization, and different modes of inducibility of their expression by extracellular stimuli. This gene maps in a region that contains the BRCA1 locus which confers susceptibility to breast and ovarian cancer. Although DUSP3 is expressed in both breast and ovarian tissues, mutation screening in breast cancer pedigrees and in sporadic tumors was negative, leading to the conclusion that this gene is not BRCA1. [provided by RefSeq].
Gene References into function
- VHR, a Vaccinia virus VH1-related dual-specific protein phosphatase, is phosphorylated at Y138 by ZAP-70.
- VHR is required for cell-cycle progression as it modulates MAP kinase activation in a cell-cycle phase-dependent manner.
- deregulated expression of BRCA1-IRIS is likely to reduce dependence on normal physiological growth stimuli
- Small dual-specificity phosphatase VHR selectively dephosphorylates tyrosine-phosphorylated interferon-alpha- and beta-activated transcription factor STAT5, leading to the subsequent inhibition of STAT5 function.
- Results highlight the importance of a high intracellular Zn(2+) content and the VHR/ZAP-70/ERK1,2-associated pathways in the modulation of LNCaP prostate cancer cell growth.
- VHR can be considered as a new marker for cancer progression in cervix carcinoma and potential new target for anticancer therapy
- VHR has a direct role in the inhibition of JNK-dependent apoptosis in LNCaP cells and may therefore have a role in prostate cancer progression.
