In addition to antigen recognition by the T-cell receptor, T-cell activation requires a second signal from a costimulatory receptor, such as CD28 (MIM 186760), which interacts with B7-1 (CD80; MIM 112203) and B7-2 (CD86; MIM 601020) ligands on antigen-presenting cells. CD28 costimulation induces transcription of interleukin-2 (IL2; MIM 147680) and stabilizes newly synthesized IL2 through the activation of mitogen-activated protein kinases (MAPKs), such as ERK (e.g., MAP2K4; MIM 601335) and JNK (see MIM 601158), and the subsequent creation of AP1 transcription factor (see MIM 165160). DUSP14 is a negative regulator of CD28 signaling.[supplied by OMIM
Immunogen
DUSP14 (NP_008957.1, 1 a.a. ~ 198 a.a) full-length human protein.
Anti-DUSP14 antibody produced in mouse is suitable for indirect immunofluorescence and western blot assay.
Biochem/physiol Actions
DUSP14 (Dual specificity phosphatase 14) is associated with several critical signaling pathways. It has ability to dephosphorylate both phosphotyrosine and phosphoserine/phosphothreonine residues on substrates. DUSP14 controls MAPK (mitogen-activated protein kinase) signaling pathway by dephosphorylating MAPK proteins ERK (extracellular-signal-regulated kinase), JNK (c-Jun N-terminal kinase) and p38. It has been reported that DUSP14 participates in T cell proliferation as a negative-feedback regulator.
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The Biochemical journal, 418(3), 475-489 (2009-02-21)
DUSPs (dual-specificity phosphatases) are a heterogeneous group of protein phosphatases that can dephosphorylate both phosphotyrosine and phosphoserine/phosphothreonine residues within the one substrate. DUSPs have been implicated as major modulators of critical signalling pathways that are dysregulated in various diseases. DUSPs
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Recent studies have demonstrated that miRNAs play a vital role in regulating myocardial ischemia/reperfusion injury (MIRI). MiR-217 has been proven to be implicated in cardiac diseases such as chronic heart failure and cardiac myxoma. However, the role of miR-217 in
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