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Validated All-in-One™ qPCR Primer for DUSP1(NM_004417.3) Search again
Product ID:
HQP004498
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
CL100, HVH1, MKP-1, MKP1, PTPN10
Gene Description:
dual specificity phosphatase 1
Target Gene Accession:
NM_004417.3(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:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
The expression of DUSP1 gene is induced in human skin fibroblasts by oxidative/heat stress and growth factors. It specifies a protein with structural features similar to members of the non-receptor-type protein-tyrosine phosphatase family, and which has significant amino-acid sequence similarity to a Tyr/Ser-protein phosphatase encoded by the late gene H1 of vaccinia virus. The bacterially expressed and purified DUSP1 protein has intrinsic phosphatase activity, and specifically inactivates mitogen-activated protein (MAP) kinase in vitro by the concomitant dephosphorylation of both its phosphothreonine and phosphotyrosine residues. Furthermore, it suppresses the activation of MAP kinase by oncogenic ras in extracts of Xenopus oocytes. Thus, DUSP1 may play an important role in the human cellular response to environmental stress as well as in the negative regulation of cellular proliferation. [provided by RefSeq].
Gene References into function
- CL100 down regulation is associated with advanced stages of epithelial ovarian neoplasms
- glucocorticoids synergistically enhance NTHi-induced TLR2 expression via specific up-regulation of the MAPK phosphatase-1 (MKP-1) that, in turn, leads to dephosphorylation and inactivation of p38 MAPK
- Data suggest that mitogen-activated protein kinase phosphatase 1 (MKP-1) participates in a negative-feedback loop which regulates p38 function and that dexamethasone may inhibit proinflammatory gene expression in part by inducing MKP-1 expression.
- Expression of MKP-1 may be associated with shorter progression-free survival times
- role of activation on cAMP-dependent protein kinase enhancement of CYP17 transcription
- our data suggest that deletion of the hv3005 and the 3-30.3 genes may predispose individual SLE patients to the development of lupus nephritis
- MKP1 is a transcriptional target of p53 involved in cell cycle regulation
- Cardiopulmonary bypass reduces ERK1/2 and p38 activity in peripheral tissue, potentially by MKP-1.
- requirement of MAPK phosphatase-1 induction and therefore, inhibition of p38 MAPK in the ANP-mediated inhibition of TNF-alpha-induced expression of MCP-1
- Jak2 is required for Ang II-induced ERK2 inactivation via induction of MKP-1 gene expression.
- Here we found that hypoxia induces MKP-1 expression in human hepatoma cells HepG2 in a time-dependent manner.
- the molecular mechanisms underlying the survival function of NGF in CESS B cell line predominantly consist in maintaining elevated levels of MKP-1 protein, which controls p38 MAPK activation.
- The expression of MKP-1 in gastric cancer cell line was elevated under hypoxia, which could downregulate the hypoxia-inducible factor 1 trans-activition activity thereby repressing the expression of downstream target vascular endothelial growth factor.
- CL100/MKP-1 has a role in progression of non-small cell lung cancer
- Prevalent MKP-1 expression in renal cell carcinoma contributes to cancer cell survival by attenuating an apoptosis inducing signal cascade via JNK.
- expression of the CL-100 phosphatase and its subsequent regulation of ERK activity play a key regulatory role in the thrombin signaling pathway
- MKP-1 induction may be antiapoptotic om breast epithelial cells and a breast cancer cell line.
- Rat ANP induces MKP-1 via endothelial Rac1 and Nox/Nox2.
- Glucocorticoid receptor-induced MPK-1 expression inhibits paclitaxel-associated MAPK activation and contributes to breast cancer cell survival
- MKP-1 is an important mediator of endotoxin tolerance via p38 regulation
- preheating accelerates MAP kinase inactivation after a second heat shock, which is related to a HSP70-mediated increase in p-MKP-1
- DNA damage in transcribed genes induces apoptosis via the JNK pathway and MKP-1.
- Hypoxia-induced MKP-1 protects overactivation of hypoxia-inducible factor 1 activation through inhibiting ERK kinase activity.
- A molecular target of macrophage migration inhibitory factor - glucocorticoid crosstalk.
- MKP-1 proteolysis can be achieved via ERK and SCF(Skp2) cooperation, thereby sustaining ERK activation
- data suggest that MKP-1, a negative regulator of ERK1/2, plays a proapoptotic role in oxidative stress-induced cell death in neuroblastoma SH-SY5Y cell line
- The MKP-1 expression in HCC (hepatocellular carcinoma) was an independent prognostic factor for outcome in HCC patients.
- Anandamide-induced rapid MKP-1 expression switches off MAPK signal transduction in microglial cells activated by stimulation of pattern recognition receptors.
- MKP-1 is required for cisplatin resistance in tumor cells.
- DUSP1 is a central regulator of innate immunity, and its expression can profoundly affect the outcome of inflammatory challenges.[review]
- These results suggest the existence of an ERK1/2-driven negative feed-back regulation of ERK5 signaling in epidermal growth factor-stimulated HK-2 cells, which is mediated by MKP-3, DUSP5 and/or MKP-1.
- In human mesangial cells, connective tissue growth factor induces the rapid transcriptional activation and synthesis of MKP-1 (MAPK phosphatase-1), a dual specificity phosphatase that dephosphorylates p38 MAPK.
- E2F-1 is a transcriptional activator of DUSP1 and DUSP1 is a link between E2F-1 and MAP kinases
- The transcription factor ATF2, which is phosphorylated and activated by JNK, is a critical mediator for inducible expression of DUSP1 and DUSP10 in this signaling pathway.
- Data suggest that JNK activation and decreased expression of MKP-1 may play important roles in progression of urothelial carcinoma.
- Regulation of ERK by MKP-1 provides a novel mechanism for control of osteoblast proliferation by glucocorticoids
- Ethanol-induced oxidative stress enhanced the tyrosine phosphorylation of PKCdelta, which in turn caused the proteasomal degradation of MKP-1, leading to sustained JNK activation and increased apoptosis in VL-17A cells.
- Distinct MAPK signaling pathways for thrombin versus VEGF induction of MKP-1 in endothelial cells. MKP-1 induction important in VEGF-stimulated endothelial cell migration.
- MKP-1 plays a critical role in ERK-mediated cisplatin resistance in ovarian carcinoma cells.
- in patients with rheumatic heart disease and heart failure MKP-1 activity was depressed in class IV patients compared to those in classes II and III
- a novel, stimulus-specific, and phosphatase-specific mechanism of ERK2 regulation in the nucleus by DUSP1, -2, and -4.
- corticosteroid-induced MKP-1 contributes to the repression of IL-6 secretion in ASM cells.
- overexpression of MKP-1 has no significant effect on Ton EBP/OREBP activity. This paradox is explained by opposing effects of p38alpha and p38delta, both of which are activated by high NaCl and inhibited by MKP-1.
- These findings indicate that p53 is a transcriptional regulator of DUSP1 in stress responses.
- distinct phosphorylation of PKCdelta on tyrosines 64 and 187 specifically activates the Erk1/2 pathway by the down-regulation of MKP-1, resulting in the persistent phosphorylation of Erk1/2 and cell apoptosis
- Glucocorticoid regulation of CD38 expression in human airway smooth muscle cells: role of dual specificity phosphatase 1
- phosphorylated heat shock protein 27 up-regulated the levels of p38 mitogen-activated protein kinase and mitogen-activated protein kinase phosphatase-1, an inhibitory protein of extracellular signal-regulated kinase
- MKP-1 upregulation by oxidative stress is potently influenced by increased mRNA stability and translation, mediated at least in part by the RNA-binding proteins HuR and NF90.
- DUSP1 reactivation led to suppression of ERK, CKS1, and SKP2 activity, inhibition of proliferation and induction of apoptosis in human hepatoma cell lines
- whether MAP kinase phosphatase (MKP)-1, a negative regulator of p38 and JNK, mediates the antiinflammatory effects of shear stress.
- High level of mitogen-activated protein kinase phosphatase-1 expression is associated with cisplatin resistance in osteosarcoma
- pneumolysin selectively induced expression of MKP1 via a TLR4-dependent MyD88-TRAF6-ERK pathway, which inhibited the PAK4-JNK signaling pathway,leading to up-regulation of MUC5AC mucin production
- The MAP kinase phosphatase-1 MKP-1/DUSP1 is a regulator of human liver response to transplantation.