Role of Dual Specificity Phosphatase in Stress and Starch Metabolism

2020 ◽  
pp. 331-351
Author(s):  
Kanwaljeet Kaur ◽  
Manas Kumar Tripathy ◽  
Girdhar K. Pandey
Keyword(s):  
Starch Metabolism ◽  
Dual Specificity Phosphatase ◽  
Dual Specificity

scholarly journals Role of CL-100, a Dual Specificity Phosphatase, in Thrombin-induced Endothelial Cell Activation

2004 ◽  
Vol 279 (45) ◽  
pp. 46678-46685 ◽  
Author(s):  
Unni M. Chandrasekharan ◽  
Lin Yang ◽  
Alicia Walters ◽  
Philip Howe ◽  
Paul E. DiCorleto
Keyword(s):  
Endothelial Cell ◽  
Cell Activation ◽  
Endothelial Cell Activation ◽  
Dual Specificity Phosphatase ◽  
Dual Specificity

scholarly journals Downregulation of Dual-specificity phosphatase 9 promotes tumor progression and contributes to poor prognosis in colorectal cancer

2020 ◽  
Author(s):  
Zhaoyan Qiu ◽  
Ning Liang ◽  
Tao Sun ◽  
Hongyuan Xue ◽  
Tianyu Xie ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Functional Role ◽  
Cpg Island ◽  
Functional Study ◽  
Dual Specificity Phosphatase ◽  
Dual Specificity ◽  
Low Expression

Abstract Background Dual-specificity phosphatase 9 (DUSP9) belongs to the dual-specificity protein phosphatase subfamily. Recently, increasing attention has been paid on the role of DUSP9 in a variety of cancers. However, its functional role in tumor development is still unclear, especially in colorectal cancer (CRC). Methods The functional role of DUSP9 in inhibiting the progression of CRC was verified both in vivo and in vitro using colony formation assay, EdU incorporation assay, wound healing assay, nude mice xenograft model, and et al. RNA-seq was performed to assess the gene expression profiling in SW480 cells with DUSP9 stable knockdown and shControl cells. Bisulfite sequencing (BSE) was performed to reveal methylation status of CpG island in promoter of DUSP9. Results DUSP9 was significantly down regulated in tumor tissues compared with peritumor tissues. Moreover, low DUSP9 expression in CRC was closely associated with tumor size, depth of invasion and advanced TNM stage, indicating that DUSP9 may be involved in the progression of CRC. Kaplan–Meier survival analysis showed that the overall survival (OS) and recurrence-free survival (RFS) of patients with low expression of DUSP9 were significantly shorter than that of patients with high expression of DUSP9. Functional study revealed that DUSP9 inhibited tumor migration, invasion and metastasis both in vitro and in vivo . Mechanistically, low expression of DUSP9 in CRC was caused by the upregulation of miR-1246 and hypermethylation status of CpG island in promoter of DUSP9. Conclusion Our findings demonstrate that DUSP9 plays a critical role in the progression of CRC and therapeutic intervention to increase the expression or activity of DUSP9 may be a potential target for CRC treatment in the future.

Abstract 508: The Role of Dual Specificity Phosphatase 5 in Post Ischemic Angiogenesis

2016 ◽  
Vol 36 (suppl_1) ◽  
Author(s):  
Dawit Ayalew ◽  
Arvin Daneshmand ◽  
Hajara Quatara ◽  
Lingdan Chen ◽  
Ayotunde O Dokun
Keyword(s):  
Endothelial Cells ◽  
Serum Starvation ◽  
Endothelial Cell Function ◽  
Dual Specificity Phosphatase ◽  
Knock Down ◽  
Simulated Ischemia ◽  
Hind Limbs ◽  
Dual Specificity ◽  
Significant Change

Background: Dual specificity phosphatase 5 (DUSP5) is a member of the protein phosphatase subfamily that inactivate their target kinases by dephosphorylating both the phosphoserine/threonine and phosphotyrosine residues. DUSP5 regulates the mitogen activated protein (MAP) kinase ERK1/2, and although it has been shown to play a key role in embryonic vascular development, its role in post ischemic angiogenesis is not known. This study sort to investigate the role of DUSP5 is endothelial cell function and angiogenesis in ischemia. Methods: Hindlimb ischemia (HLI) was induced in mice and at day 3 post HLI, expression of DUSP5 was assessed in the ischemic hind limbs. We assessed DUSP5 expression in 3 major cell types found the ischemic hindlimb, endothelial cells or ECs (human umbilical vein endothelial cells, HUVECs), skeletal muscle myoblast (C2C12) and vascular smooth muscles cells (VSMC). Cells were exposed to simulated ischemia (2% oxygen with serum starvation) for 24 hours analyzed for DUSP5 mRNA and protein expression. The effect of loss of DUSP5 on EC function in ischemia was assessed by CRISPR/Cas9 mediated knock down of DUSP5 followed by analysis of EC proliferation, apoptosis and tube formation in simulated ischemia. Results: DUSP5 protein levels were significantly upregulated in mouse post ischemic hind limbs (ischemic (I) vs non-ischemic (NI); 1.63 ± 0.39 vs. 0.22 ± 0.02, p<0.05, n=3). Post ischemic exposure, ECs and C2C12 showed significant upregulation of DUSP5 protein. (DUSP5/Tubulin, I vs NI, HUVEC: 0.43 ± 0.09 vs. 0.09 ± 0.03, p<0.02; C2C12: 1.77 ± 0.10 vs. 0.42 ± 0.01, p< 0.01, n=5). VSMCs showed no significant change in DUSP5 expression. Knock down of DUSP5 in HUVECs resulted in significant decrease in cell proliferation in ischemia (O.D 450 control vs knock-down : 0.46 ± 0.01 vs. 0.34 ± 0.01, p<0.01, n=7) but no significant change in apoptosis (O.D 450 control vs knock-down: 0.13 ± 0.01 vs. 0.13 ± 0.00, p>0.05, n=7). It also resulted in significant impairment in, in vitro angiogenesis (tube/sq cm: 28.6 ± 1.2 vs. 16.43 ± 1.6, p<0.01, n=7). Conclusion: DUSP5 is highly upregulated in ischemic endothelial cells and plays an important role in EC proliferation and post ischemic angiogenesis.

scholarly journals Structural Insight into the Critical Role of the N-Terminal Region in the Catalytic Activity of Dual-Specificity Phosphatase 26

PLoS ONE ◽  
2016 ◽  
Vol 11 (9) ◽  
pp. e0162115 ◽  
Author(s):  
Eun-Young Won ◽  
Sang-Ok Lee ◽  
Dong-Hwa Lee ◽  
Daeyoup Lee ◽  
Kwang-Hee Bae ◽  
...  
Keyword(s):  
Catalytic Activity ◽  
Critical Role ◽  
Terminal Region ◽  
Dual Specificity Phosphatase ◽  
Dual Specificity ◽  
Structural Insight ◽  
Insight Into

scholarly journals The Dual-Specificity Phosphatase 10 (DUSP10): Its Role in Cancer, Inflammation, and Immunity

2019 ◽  
Vol 20 (7) ◽  
pp. 1626 ◽  
Author(s):  
Marta Jiménez-Martínez ◽  
Konstantinos Stamatakis ◽  
Manuel Fresno
Keyword(s):  
Developed Countries ◽  
Dual Specificity Phosphatase ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signals ◽  
Dual Specificity ◽  
Extracellular Signal ◽  
The Family ◽  
Mitogen Activated Protein ◽  
Cancer And Inflammation

Cancer is one of the most diagnosed diseases in developed countries. Inflammation is a common response to different stress situations including cancer and infection. In those processes, the family of mitogen-activated protein kinases (MAPKs) has an important role regulating cytokine secretion, proliferation, survival, and apoptosis, among others. MAPKs regulate a large number of extracellular signals upon a variety of physiological as well as pathological conditions. MAPKs activation is tightly regulated by phosphorylation/dephosphorylation events. In this regard, the dual-specificity phosphatase 10 (DUSP10) has been described as a MAPK phosphatase that negatively regulates p38 MAPK and c-Jun N-terminal kinase (JNK) in several cellular types and tissues. Several studies have proposed that extracellular signal-regulated kinase (ERK) can be also modulated by DUSP10. This suggests a complex role of DUSP10 on MAPKs regulation and, in consequence, its impact in a wide variety of responses involved in both cancer and inflammation. Here, we review DUSP10 function in cancerous and immune cells and studies in both mouse models and patients that establish a clear role of DUSP10 in different processes such as inflammation, immunity, and cancer.

scholarly journals The catalytic role of Cys124 in the dual specificity phosphatase VHR.

1994 ◽  
Vol 269 (45) ◽  
pp. 28084-28090
Author(s):  
G Zhou ◽  
J M Denu ◽  
L Wu ◽  
J E Dixon
Keyword(s):  
Dual Specificity Phosphatase ◽  
Dual Specificity ◽  
Catalytic Role

Role of Conserved Histidine and Serine in the HCXXXXXRS Motif of Human Dual-Specificity Phosphatase 5

2019 ◽  
Vol 59 (4) ◽  
pp. 1563-1574
Author(s):  
Ankan Gupta ◽  
Jaladhi Brahmbhatt ◽  
Raulia Syrlybaeva ◽  
Catherine Bodnar ◽  
Natalia Bodnar ◽  
...  
Keyword(s):  
Dual Specificity Phosphatase ◽  
Dual Specificity

scholarly journals Dual specificity phosphatase 6 as a predictor of invasiveness in papillary thyroid cancer

2012 ◽  
Vol 167 (1) ◽  
pp. 93-101 ◽  
Author(s):  
Jung Uee Lee ◽  
Songmei Huang ◽  
Min Hee Lee ◽  
Seong Eun Lee ◽  
Min Jeong Ryu ◽  
...  
Keyword(s):  
High Risk ◽  
Staining Intensity ◽  
Benign Neoplasms ◽  
Papillary Thyroid ◽  
Mutation Status ◽  
Dual Specificity Phosphatase ◽  
Dual Specificity ◽  
And Migration ◽  
Transcriptional Output

ObjectiveThe genetic mutations causing the constitutive activation of MEK/ERK have been regarded as an initiating factor in papillary thyroid carcinoma (PTC). The ERK-specific dual specificity phosphatase 6 (DUSP6) is part of the ERK-dependent transcriptional output. Therefore, the coordinated regulation of the activities of ERK kinases and DUSP6 may need to be reestablished to make new balances in PTC.MethodsTo investigate the role of DUSP6 in the regulation of ERK1/2 (MAPK3/1)-dependent transcription, 42 benign neoplasms and 167 PTCs were retrospectively analyzed by immunohistochemistry with dideoxy sequencing to detect BRAFV600E mutation.ResultsThe expressions of total ERK1/2, DUSP6, c-Fos (FOS), c-Myc (MYC), cyclin D1, and PCNA were markedly increased in PTC compared with those in benign neoplasms. However, phospho-ERK1/2 was detected in only eight (4.8%) cases out of 167 PTC samples. Unexpectedly, the staining intensity and nuclear localization of ERK1/2 were not affected by the presence or absence of the BRAFV600E mutation. However, the expressions of c-Fos and PCNA were elevated in BRAFV600E-positive PTC compared with those in BRAFV600E-negative PTC. Interestingly, the higher staining intensities of DUSP6 were associated with the level of total ERK1/2 expression (P=0.04) and with high-risk biological features such as age (P=0.05), tumor size (P=0.01), and extrathyroidal extension (linear by linear association, P=0.02). In addition, DUSP6 silencing significantly decreased the cell viability and migration rate of FRO cells.ConclusionsThe coordinated upregulation of total ERK1/2 and its phosphatase, DUSP6, is related to bare detection of phospho-ERK1/2 in PTC regardless of BRAFV600E mutation status. A link between DUSP6 expression and high-risk features of PTC suggested that DUSP6 is an important independent factor affecting the signaling pathways in established PTC.

THE ROLE OF DUSP22 (DUAL SPECIFICITY PHOSPHATASE 22) GENE EXPRESSION IN THE PROGNOSIS OF LOW GRADE LYMPHOMAS

2019 ◽  
Vol 37 ◽  
pp. 340-341 ◽  
Author(s):  
S. Paydas ◽  
E.K. Bagir ◽  
M. Ergin ◽  
G. Seydaoglu ◽  
A. Boz
Keyword(s):  
Gene Expression ◽  
Low Grade ◽  
Dual Specificity Phosphatase ◽  
Dual Specificity
Sign in / Sign up

Export Citation Format

Share Document