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Gene Symbol |
PKN2 |
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Aliases |
PAK2, PRK2, PRKCL2, PRO2042, Pak-2, STK7 |
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Entrez Gene ID |
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Gene Name |
Protein kinase N2 |
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Chromosomal Location |
1p22.2 |
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HGNC ID |
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e!Ensembl
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| Protein Information |
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Protein Name |
Serine/threonine-protein kinase N2, PKN gamma, cardiolipin-activated protein kinase Pak2, protein kinase C-like 2, protein-kinase C-related kinase 2 |
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Function |
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PKC-related serine/threonine-protein kinase and Rho/Rac effector protein that participates in specific signal transduction responses in the cell. Plays a role in the regulation of cell cycle progression, actin cytoskeleton assembly, cell migration, cell adhesion, tumor cell invasion and transcription activation signaling processes. Phosphorylates CTTN in hyaluronan-induced astrocytes and hence decreases CTTN ability to associate with filamentous actin. Phosphorylates HDAC5, therefore lead to impair HDAC5 import. Direct RhoA target required for the regulation of the maturation of primordial junctions into apical junction formation in bronchial epithelial cells. Required for G2/M phases of the cell cycle progression and abscission during cytokinesis in a ECT2-dependent manner. Stimulates FYN kinase activity that is required for establishment of skin cell-cell adhesion during keratinocytes differentiation. Regulates epithelial bladder cells speed and direction of movement during cell migration and tumor cell invasion. Inhibits Akt pro-survival-induced kinase activity. Mediates Rho protein-induced transcriptional activation via the c-fos serum response factor (SRF). Involved in the negative regulation of ciliogenesis (PubMed:27104747). .; (Microbial infection) Phosphorylates HCV NS5B leading to stimulation of HCV RNA replication. |
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UniProt |
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PDB |
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Interactions |
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| STRING |
MINT |
IntAct |
| ENSP00000348069 |
P36956 |
P36956 |
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View interactions
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Associated Diseases
| Disease group | Disease Name | References |
| Endocrine System Diseases |
| PCOS |
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| Neoplasms |
| Breast Cancer |
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| Nervous System Diseases |
| Huntington Disease |
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References |
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| Corton Marta, Botella-Carretero Jose I, Benguria Alberto, Villuendas Gemma, Zaballos Angel, San Millan Jose L, Escobar-Morreale Hector F, Peral Belen |
| Instituto de Investigaciones Biomedicas, Consejo Superior de Investigaciones Cientificas and Universidad Autonoma de Madrid, E-28029 Madrid, Spain. |
| J Clin Endocrinol Metab. 2007 Jan;92(1):328-37. doi: 10.1210/jc.2006-1665. Epub |
Abstract
CONTEXT: The polycystic ovary syndrome (PCOS) is frequently associated with visceral obesity, suggesting that omental adipose tissue might play an important role in the pathogenesis of the syndrome. OBJECTIVE: The objective was to study the expression profiles of omental fat biopsy samples obtained from morbidly obese women with or without PCOS at the time of bariatric surgery. DESIGN: This was a case-control study. SETTINGS: We conducted the study in an academic hospital. PATIENTS: Eight PCOS patients and seven nonhyperandrogenic women submitted to bariatric surgery because of morbid obesity. INTERVENTIONS: Biopsy samples of omental fat were obtained during bariatric surgery. MAIN OUTCOME MEASURE: The main outcome measure was high-density oligonucleotide arrays. RESULTS: After statistical analysis, we identified changes in the expression patterns of 63 genes between PCOS and control samples. Gene classification was assessed through data mining of Gene Ontology annotations and cluster analysis of dysregulated genes between both groups. These methods highlighted abnormal expression of genes encoding certain components of several biological pathways related to insulin signaling and Wnt signaling, oxidative stress, inflammation, immune function, and lipid metabolism, as well as other genes previously related to PCOS or to the metabolic syndrome. CONCLUSION: The differences in the gene expression profiles in visceral adipose tissue of PCOS patients compared with nonhyperandrogenic women involve multiple genes related to several biological pathways, suggesting that the involvement of abdominal obesity in the pathogenesis of PCOS is more ample than previously thought and is not restricted to the induction of insulin resistance. |
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