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Validated All-in-One™ qPCR Primer for PPM1D(NM_003620.3) Search again
Product ID:
HQP021053
(click here to view gene annotation page)
Species:
Human
Symbol:
Alias:
IDDGIP, JDVS, PP2C-DELTA, WIP1
Gene Description:
protein phosphatase, Mg2+/Mn2+ dependent 1D
Target Gene Accession:
NM_003620.3(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:
Summary
The protein encoded by this gene is a member of the PP2C family of Ser/Thr protein phosphatases. PP2C family members are known to be negative regulators of cell stress response pathways.
Gene References into function
- Functional study of the mouse homolog
- PPM1D, encoding a serine/threonine protein phosphatase, lies within an epicenter of the region at 17q23, is amplified in breast cancer
- PPM1D amplification contributes to the development of human cancers by suppressing p53 activation
- ablation of gene confers resistance to breast tumors induced by certain oncogenes
- Data demonstrate that p53-induced phosphatase PPM1D interacts with the nuclear isoform of uracil DNA glycosylase, UNG2, and suppresses base excision repair.
- suggest that substrate recognition by Wip1 is centered toward a very narrow region around the pTXpY sequence
- Primary function of PPM1D is to reverse the p53 and Chk1-induced DNA damage and cell cycle checkpoint responses and return the cell to a homeostatic state following completion of DNA repair.
- PPM1D is frequently activated through amplification in aggressive primary breast tumours
- Wip1 acts as a negative regulator of Chk2 and inhibition of Wip1 expression by RNA interference results in abnormally sustained Thr68 phosphorylation of Chk2.
- Increased protein-levels of PPM1D may link the TP53 and RB1 tumor suppressor pathways to medulloblastoma pathomechanisms.
- Demonstrated the ability of protein phosphatase 1D magnesium-dependent, delta isoform (PPM1D) to positively modulate the activity of type I and II nuclear receptors.
- PPM1D promotes breast tumor growth both by inhibiting p53 activity and by enhancing steroid hormone receptor action
- an intrinsic kinase activity of Chk2, but not phosphatase activity of Wip1, is required for the association of fulllength Chk2 and Wip1
- Wip1 overexpression abrogates the homeostatic balance maintained through the p38-p53-Wip1 pathway, and contributes to malignant progression by inactivating wild-type p53 and p38 MAPK as well as decreasing p16 protein levels in human breast tissues.
- E2F and Wip1 are modulators of E2F1-induced apoptosis involving p38 MAP kinase
- These results indicate that Wip1 is one of the phosphatases regulating the activity of Chk2 in response to DNA damage.
- Wip1 phosphatase is an integral component of an ATM-dependent signaling pathway.
- Operates within the map kinase kinase 6/p38 map kinase signaling pathway to promote ErbB2-driven mammary gland tumorigenesis in transgenic mice.
- WIP1 is expressed in non-neoplastic gastric mucosa and is frequently overexpressed in gastric cancers.
- Wip1 acts as a gatekeeper in the Mdm2-p53 regulatory loop by stabilizing Mdm2 and promoting Mdm2-mediated proteolysis of p53.
- The Wip1 phosphatase PPM1D dephosphorylates SQ/TQ motifs in checkpoint substrates phosphorylated by PI3K-like kinases.
- PPM1D contributes to breast cancer associated phenotypic characteristics by directly or indirectly affecting several important cellular signaling pathways.
- Our findings demonstrate that PPM1D is involved in the regulation of cell proliferation in breast cancer in a p53-dependent manner and that overexpression of PPM1D contributes to malignant phenotype by promoting sustained cell growth and cell survival.
- ATO-induced activation of Chk2/p53 and p38 MAPK/p53 apoptotic pathways can be enhanced by siRNA-mediated suppression of Wip1 expression, further indicating that ATO inhibits Wip1 phosphatase in vivo
- identification of the active center and further elucidation of the substrate preference of PPM1D; findings showed that the putative active site residues of PPM1D are highly conserved among the PPM1 family members
- Characterization of a conserved p53 response element located in the 5' untranslated region of the PPM1D gene that is required for the p53-dependent induction of transcription from the human PPM1D promoter.
