MAPK Phosphatase-1 (MKP-1) Expression Is Up-Regulated by hCG/cAMP and Modulates Steroidogenesis in MA-10 Leydig Cells
MAP kinases (MAPKs), such as ERK1/2, exert profound effects on a variety of physiological processes. In steroidogenic cells, ERK1/2 are involved in the expression and activation of steroidogenic acute regulatory protein, which plays a central role in the regulation of steroidogenesis. In MA-10 Leydi...
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creator | Brion, Laura Maloberti, Paula M Gomez, Natalia V Poderoso, Cecilia Gorostizaga, Alejandra B Mori Sequeiros Garcia, Maria M Acquier, Andrea B Cooke, Mariana Mendez, Carlos F Podesta, Ernesto J Paz, Cristina |
description | MAP kinases (MAPKs), such as ERK1/2, exert profound effects on a variety of physiological processes. In steroidogenic cells, ERK1/2 are involved in the expression and activation of steroidogenic acute regulatory protein, which plays a central role in the regulation of steroidogenesis. In MA-10 Leydig cells, LH and chorionic gonadotropin (CG) trigger transient ERK1/2 activation via protein kinase A, although the events that lead to ERK1/2 inactivation are not fully described. Here, we describe the hormonal regulation of MAPK phosphatase-1 (MKP-1), an enzyme that inactivates MAPKs, in MA-10 cells. In our experiments, human CG (hCG)/cAMP stimulation rapidly and transiently increased MKP-1 mRNA levels by a transcriptional action. This effect was accompanied by an increase in protein levels in both nuclear and mitochondrial compartments. In cells transiently expressing flag-MKP-1 protein, hCG/cAMP promoted the accumulation of the recombinant protein in a time-dependent manner (10-fold at 1 h). Moreover, hCG/cAMP triggered ERK1/2-dependent MKP-1 phosphorylation. The blockade of cAMP-induced MAPK kinase/ERK activation abated MKP-1 phosphorylation but only partially reduced flag-MKP-1 protein accumulation. Together, these results suggest that hCG regulates MKP-1 at transcriptional and posttranslational level, protein phosphorylation being one of the mechanisms involved in this regulation. Our study also demonstrates that MKP-1 overexpression reduces the effects of cAMP on ERK1/2 phosphorylation, steroidogenic acute regulatory gene promoter activity, mRNA levels, and steroidogenesis, whereas MKP-1 down-regulation by small interfering RNA produces opposite effects. In summary, our data demonstrate that hCG regulates MKP-1 expression at multiple stages as a negative feedback regulatory mechanism to modulate the hormonal action on ERK1/2 activity and steroidogenesis. |
doi_str_mv | 10.1210/en.2011-0021 |
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In steroidogenic cells, ERK1/2 are involved in the expression and activation of steroidogenic acute regulatory protein, which plays a central role in the regulation of steroidogenesis. In MA-10 Leydig cells, LH and chorionic gonadotropin (CG) trigger transient ERK1/2 activation via protein kinase A, although the events that lead to ERK1/2 inactivation are not fully described. Here, we describe the hormonal regulation of MAPK phosphatase-1 (MKP-1), an enzyme that inactivates MAPKs, in MA-10 cells. In our experiments, human CG (hCG)/cAMP stimulation rapidly and transiently increased MKP-1 mRNA levels by a transcriptional action. This effect was accompanied by an increase in protein levels in both nuclear and mitochondrial compartments. In cells transiently expressing flag-MKP-1 protein, hCG/cAMP promoted the accumulation of the recombinant protein in a time-dependent manner (10-fold at 1 h). Moreover, hCG/cAMP triggered ERK1/2-dependent MKP-1 phosphorylation. The blockade of cAMP-induced MAPK kinase/ERK activation abated MKP-1 phosphorylation but only partially reduced flag-MKP-1 protein accumulation. Together, these results suggest that hCG regulates MKP-1 at transcriptional and posttranslational level, protein phosphorylation being one of the mechanisms involved in this regulation. Our study also demonstrates that MKP-1 overexpression reduces the effects of cAMP on ERK1/2 phosphorylation, steroidogenic acute regulatory gene promoter activity, mRNA levels, and steroidogenesis, whereas MKP-1 down-regulation by small interfering RNA produces opposite effects. In summary, our data demonstrate that hCG regulates MKP-1 expression at multiple stages as a negative feedback regulatory mechanism to modulate the hormonal action on ERK1/2 activity and steroidogenesis.</description><identifier>ISSN: 0013-7227</identifier><identifier>EISSN: 1945-7170</identifier><identifier>DOI: 10.1210/en.2011-0021</identifier><identifier>PMID: 21558315</identifier><identifier>CODEN: ENDOAO</identifier><language>eng</language><publisher>Chevy Chase, MD: Endocrine Society</publisher><subject>Accumulation ; Animals ; Biological and medical sciences ; Cell activation ; Cell Line ; Cell Nucleus - metabolism ; Chorionic gonadotropin ; Chorionic Gonadotropin - metabolism ; Cyclic AMP ; Cyclic AMP - metabolism ; Dual Specificity Phosphatase 1 - antagonists & inhibitors ; Dual Specificity Phosphatase 1 - genetics ; Dual Specificity Phosphatase 1 - metabolism ; Extracellular signal-regulated kinase ; Flags ; Fundamental and applied biological sciences. Psychology ; Gene expression ; Gene regulation ; Genes, Reporter ; Gonadotropins ; Inactivation ; Kinases ; Leydig cells ; Leydig Cells - cytology ; Leydig Cells - metabolism ; Male ; MAP kinase ; MAP kinase phosphatase ; MAP Kinase Signaling System - drug effects ; Mice ; Mitochondria - metabolism ; MKP-1 protein ; Negative feedback ; Phosphatase ; Phosphoproteins - genetics ; Phosphoproteins - metabolism ; Phosphorylation ; Phosphorylation - drug effects ; Physiological effects ; Pituitary (anterior) ; Promoter Regions, Genetic ; Protein folding ; Protein kinase A ; Protein Kinase Inhibitors - pharmacology ; Protein Processing, Post-Translational - drug effects ; Proteins ; Recombinant Fusion Proteins - metabolism ; Regulatory mechanisms (biology) ; RNA, Messenger - metabolism ; RNA, Small Interfering ; siRNA ; Steroidogenesis ; Steroidogenic acute regulatory protein ; Transcriptional Activation - drug effects ; Vertebrates: endocrinology</subject><ispartof>Endocrinology (Philadelphia), 2011-07, Vol.152 (7), p.2665-2677</ispartof><rights>Copyright © 2011 by The Endocrine Society</rights><rights>Copyright © 2011 by The Endocrine Society 2011</rights><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c528t-b2893a808ef20766173ac327573341f37cce043ed09fa4b43e8a2383003474943</citedby><cites>FETCH-LOGICAL-c528t-b2893a808ef20766173ac327573341f37cce043ed09fa4b43e8a2383003474943</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=24275790$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21558315$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Brion, Laura</creatorcontrib><creatorcontrib>Maloberti, Paula M</creatorcontrib><creatorcontrib>Gomez, Natalia V</creatorcontrib><creatorcontrib>Poderoso, Cecilia</creatorcontrib><creatorcontrib>Gorostizaga, Alejandra B</creatorcontrib><creatorcontrib>Mori Sequeiros Garcia, Maria M</creatorcontrib><creatorcontrib>Acquier, Andrea B</creatorcontrib><creatorcontrib>Cooke, Mariana</creatorcontrib><creatorcontrib>Mendez, Carlos F</creatorcontrib><creatorcontrib>Podesta, Ernesto J</creatorcontrib><creatorcontrib>Paz, Cristina</creatorcontrib><title>MAPK Phosphatase-1 (MKP-1) Expression Is Up-Regulated by hCG/cAMP and Modulates Steroidogenesis in MA-10 Leydig Cells</title><title>Endocrinology (Philadelphia)</title><addtitle>Endocrinology</addtitle><description>MAP kinases (MAPKs), such as ERK1/2, exert profound effects on a variety of physiological processes. In steroidogenic cells, ERK1/2 are involved in the expression and activation of steroidogenic acute regulatory protein, which plays a central role in the regulation of steroidogenesis. In MA-10 Leydig cells, LH and chorionic gonadotropin (CG) trigger transient ERK1/2 activation via protein kinase A, although the events that lead to ERK1/2 inactivation are not fully described. Here, we describe the hormonal regulation of MAPK phosphatase-1 (MKP-1), an enzyme that inactivates MAPKs, in MA-10 cells. In our experiments, human CG (hCG)/cAMP stimulation rapidly and transiently increased MKP-1 mRNA levels by a transcriptional action. This effect was accompanied by an increase in protein levels in both nuclear and mitochondrial compartments. In cells transiently expressing flag-MKP-1 protein, hCG/cAMP promoted the accumulation of the recombinant protein in a time-dependent manner (10-fold at 1 h). Moreover, hCG/cAMP triggered ERK1/2-dependent MKP-1 phosphorylation. The blockade of cAMP-induced MAPK kinase/ERK activation abated MKP-1 phosphorylation but only partially reduced flag-MKP-1 protein accumulation. Together, these results suggest that hCG regulates MKP-1 at transcriptional and posttranslational level, protein phosphorylation being one of the mechanisms involved in this regulation. Our study also demonstrates that MKP-1 overexpression reduces the effects of cAMP on ERK1/2 phosphorylation, steroidogenic acute regulatory gene promoter activity, mRNA levels, and steroidogenesis, whereas MKP-1 down-regulation by small interfering RNA produces opposite effects. In summary, our data demonstrate that hCG regulates MKP-1 expression at multiple stages as a negative feedback regulatory mechanism to modulate the hormonal action on ERK1/2 activity and steroidogenesis.</description><subject>Accumulation</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cell activation</subject><subject>Cell Line</subject><subject>Cell Nucleus - metabolism</subject><subject>Chorionic gonadotropin</subject><subject>Chorionic Gonadotropin - metabolism</subject><subject>Cyclic AMP</subject><subject>Cyclic AMP - metabolism</subject><subject>Dual Specificity Phosphatase 1 - antagonists & inhibitors</subject><subject>Dual Specificity Phosphatase 1 - genetics</subject><subject>Dual Specificity Phosphatase 1 - metabolism</subject><subject>Extracellular signal-regulated kinase</subject><subject>Flags</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene expression</subject><subject>Gene regulation</subject><subject>Genes, Reporter</subject><subject>Gonadotropins</subject><subject>Inactivation</subject><subject>Kinases</subject><subject>Leydig cells</subject><subject>Leydig Cells - cytology</subject><subject>Leydig Cells - metabolism</subject><subject>Male</subject><subject>MAP kinase</subject><subject>MAP kinase phosphatase</subject><subject>MAP Kinase Signaling System - drug effects</subject><subject>Mice</subject><subject>Mitochondria - metabolism</subject><subject>MKP-1 protein</subject><subject>Negative feedback</subject><subject>Phosphatase</subject><subject>Phosphoproteins - genetics</subject><subject>Phosphoproteins - metabolism</subject><subject>Phosphorylation</subject><subject>Phosphorylation - drug effects</subject><subject>Physiological effects</subject><subject>Pituitary (anterior)</subject><subject>Promoter Regions, Genetic</subject><subject>Protein folding</subject><subject>Protein kinase A</subject><subject>Protein Kinase Inhibitors - pharmacology</subject><subject>Protein Processing, Post-Translational - drug effects</subject><subject>Proteins</subject><subject>Recombinant Fusion Proteins - metabolism</subject><subject>Regulatory mechanisms (biology)</subject><subject>RNA, Messenger - metabolism</subject><subject>RNA, Small Interfering</subject><subject>siRNA</subject><subject>Steroidogenesis</subject><subject>Steroidogenic acute regulatory protein</subject><subject>Transcriptional Activation - drug effects</subject><subject>Vertebrates: endocrinology</subject><issn>0013-7227</issn><issn>1945-7170</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kd9v0zAQxy0EYqXwtufJEkKAhLfzj9TJY1V1Y1ojKmDPketc2kypndmJRP_7pWuhEoKnu5M_uvt-_SXknMMlFxyu0F0K4JwBCP6CjHimEqa5hpdkBMAl00LoM_ImxodhVErJ1-RM8CRJJU9GpM-nyzu63PjYbkxnIjJOP-V3S8Y_0_mvNmCMtXf0NtL7ln3Hdd-YDku62tHN7ObKTvMlNa6kuS-fXyL90WHwdenX6DDWkdaO5lPGgS5wV9ZrOsOmiW_Jq8o0Ed8d65jcX89_zr6yxbeb29l0wWwi0o6tRJpJk0KKlQA9mXAtjZVCJ1pKxSuprUVQEkvIKqNWQ5caIVMJIJVWmZJj8vGwtw3-scfYFds62kGBcej7WKRaatAJZAP5_i_ywffBDeIKySVMBmqoY_LlQNngYwxYFW2otybsCg7FPo0CXbFPo9inMeAXx6X9aovlH_j39w_AhyNgojVNFYyzdTxxau81g5MP37f_O8mOJ-WBRFd6G2qHzxme3PxT6BOAa6mD</recordid><startdate>20110701</startdate><enddate>20110701</enddate><creator>Brion, Laura</creator><creator>Maloberti, Paula M</creator><creator>Gomez, Natalia V</creator><creator>Poderoso, Cecilia</creator><creator>Gorostizaga, Alejandra B</creator><creator>Mori Sequeiros Garcia, Maria M</creator><creator>Acquier, Andrea B</creator><creator>Cooke, Mariana</creator><creator>Mendez, Carlos F</creator><creator>Podesta, Ernesto J</creator><creator>Paz, Cristina</creator><general>Endocrine Society</general><general>Oxford University Press</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QG</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>20110701</creationdate><title>MAPK Phosphatase-1 (MKP-1) Expression Is Up-Regulated by hCG/cAMP and Modulates Steroidogenesis in MA-10 Leydig Cells</title><author>Brion, Laura ; Maloberti, Paula M ; Gomez, Natalia V ; Poderoso, Cecilia ; Gorostizaga, Alejandra B ; Mori Sequeiros Garcia, Maria M ; Acquier, Andrea B ; Cooke, Mariana ; Mendez, Carlos F ; Podesta, Ernesto J ; Paz, Cristina</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c528t-b2893a808ef20766173ac327573341f37cce043ed09fa4b43e8a2383003474943</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Accumulation</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cell activation</topic><topic>Cell Line</topic><topic>Cell Nucleus - metabolism</topic><topic>Chorionic gonadotropin</topic><topic>Chorionic Gonadotropin - metabolism</topic><topic>Cyclic AMP</topic><topic>Cyclic AMP - metabolism</topic><topic>Dual Specificity Phosphatase 1 - antagonists & inhibitors</topic><topic>Dual Specificity Phosphatase 1 - genetics</topic><topic>Dual Specificity Phosphatase 1 - metabolism</topic><topic>Extracellular signal-regulated kinase</topic><topic>Flags</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene expression</topic><topic>Gene regulation</topic><topic>Genes, Reporter</topic><topic>Gonadotropins</topic><topic>Inactivation</topic><topic>Kinases</topic><topic>Leydig cells</topic><topic>Leydig Cells - cytology</topic><topic>Leydig Cells - metabolism</topic><topic>Male</topic><topic>MAP kinase</topic><topic>MAP kinase phosphatase</topic><topic>MAP Kinase Signaling System - drug effects</topic><topic>Mice</topic><topic>Mitochondria - metabolism</topic><topic>MKP-1 protein</topic><topic>Negative feedback</topic><topic>Phosphatase</topic><topic>Phosphoproteins - genetics</topic><topic>Phosphoproteins - metabolism</topic><topic>Phosphorylation</topic><topic>Phosphorylation - drug effects</topic><topic>Physiological effects</topic><topic>Pituitary (anterior)</topic><topic>Promoter Regions, Genetic</topic><topic>Protein folding</topic><topic>Protein kinase A</topic><topic>Protein Kinase Inhibitors - pharmacology</topic><topic>Protein Processing, Post-Translational - drug effects</topic><topic>Proteins</topic><topic>Recombinant Fusion Proteins - metabolism</topic><topic>Regulatory mechanisms (biology)</topic><topic>RNA, Messenger - metabolism</topic><topic>RNA, Small Interfering</topic><topic>siRNA</topic><topic>Steroidogenesis</topic><topic>Steroidogenic acute regulatory protein</topic><topic>Transcriptional Activation - drug effects</topic><topic>Vertebrates: endocrinology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Brion, Laura</creatorcontrib><creatorcontrib>Maloberti, Paula M</creatorcontrib><creatorcontrib>Gomez, Natalia V</creatorcontrib><creatorcontrib>Poderoso, Cecilia</creatorcontrib><creatorcontrib>Gorostizaga, Alejandra B</creatorcontrib><creatorcontrib>Mori Sequeiros Garcia, Maria M</creatorcontrib><creatorcontrib>Acquier, Andrea B</creatorcontrib><creatorcontrib>Cooke, Mariana</creatorcontrib><creatorcontrib>Mendez, Carlos F</creatorcontrib><creatorcontrib>Podesta, Ernesto J</creatorcontrib><creatorcontrib>Paz, Cristina</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Animal Behavior Abstracts</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Endocrinology (Philadelphia)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Brion, Laura</au><au>Maloberti, Paula M</au><au>Gomez, Natalia V</au><au>Poderoso, Cecilia</au><au>Gorostizaga, Alejandra B</au><au>Mori Sequeiros Garcia, Maria M</au><au>Acquier, Andrea B</au><au>Cooke, Mariana</au><au>Mendez, Carlos F</au><au>Podesta, Ernesto J</au><au>Paz, Cristina</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MAPK Phosphatase-1 (MKP-1) Expression Is Up-Regulated by hCG/cAMP and Modulates Steroidogenesis in MA-10 Leydig Cells</atitle><jtitle>Endocrinology (Philadelphia)</jtitle><addtitle>Endocrinology</addtitle><date>2011-07-01</date><risdate>2011</risdate><volume>152</volume><issue>7</issue><spage>2665</spage><epage>2677</epage><pages>2665-2677</pages><issn>0013-7227</issn><eissn>1945-7170</eissn><coden>ENDOAO</coden><abstract>MAP kinases (MAPKs), such as ERK1/2, exert profound effects on a variety of physiological processes. In steroidogenic cells, ERK1/2 are involved in the expression and activation of steroidogenic acute regulatory protein, which plays a central role in the regulation of steroidogenesis. In MA-10 Leydig cells, LH and chorionic gonadotropin (CG) trigger transient ERK1/2 activation via protein kinase A, although the events that lead to ERK1/2 inactivation are not fully described. Here, we describe the hormonal regulation of MAPK phosphatase-1 (MKP-1), an enzyme that inactivates MAPKs, in MA-10 cells. In our experiments, human CG (hCG)/cAMP stimulation rapidly and transiently increased MKP-1 mRNA levels by a transcriptional action. This effect was accompanied by an increase in protein levels in both nuclear and mitochondrial compartments. In cells transiently expressing flag-MKP-1 protein, hCG/cAMP promoted the accumulation of the recombinant protein in a time-dependent manner (10-fold at 1 h). Moreover, hCG/cAMP triggered ERK1/2-dependent MKP-1 phosphorylation. The blockade of cAMP-induced MAPK kinase/ERK activation abated MKP-1 phosphorylation but only partially reduced flag-MKP-1 protein accumulation. Together, these results suggest that hCG regulates MKP-1 at transcriptional and posttranslational level, protein phosphorylation being one of the mechanisms involved in this regulation. Our study also demonstrates that MKP-1 overexpression reduces the effects of cAMP on ERK1/2 phosphorylation, steroidogenic acute regulatory gene promoter activity, mRNA levels, and steroidogenesis, whereas MKP-1 down-regulation by small interfering RNA produces opposite effects. In summary, our data demonstrate that hCG regulates MKP-1 expression at multiple stages as a negative feedback regulatory mechanism to modulate the hormonal action on ERK1/2 activity and steroidogenesis.</abstract><cop>Chevy Chase, MD</cop><pub>Endocrine Society</pub><pmid>21558315</pmid><doi>10.1210/en.2011-0021</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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source | MEDLINE; Journals@Ovid Ovid Autoload; Oxford University Press Journals All Titles (1996-Current); EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
subjects | Accumulation Animals Biological and medical sciences Cell activation Cell Line Cell Nucleus - metabolism Chorionic gonadotropin Chorionic Gonadotropin - metabolism Cyclic AMP Cyclic AMP - metabolism Dual Specificity Phosphatase 1 - antagonists & inhibitors Dual Specificity Phosphatase 1 - genetics Dual Specificity Phosphatase 1 - metabolism Extracellular signal-regulated kinase Flags Fundamental and applied biological sciences. Psychology Gene expression Gene regulation Genes, Reporter Gonadotropins Inactivation Kinases Leydig cells Leydig Cells - cytology Leydig Cells - metabolism Male MAP kinase MAP kinase phosphatase MAP Kinase Signaling System - drug effects Mice Mitochondria - metabolism MKP-1 protein Negative feedback Phosphatase Phosphoproteins - genetics Phosphoproteins - metabolism Phosphorylation Phosphorylation - drug effects Physiological effects Pituitary (anterior) Promoter Regions, Genetic Protein folding Protein kinase A Protein Kinase Inhibitors - pharmacology Protein Processing, Post-Translational - drug effects Proteins Recombinant Fusion Proteins - metabolism Regulatory mechanisms (biology) RNA, Messenger - metabolism RNA, Small Interfering siRNA Steroidogenesis Steroidogenic acute regulatory protein Transcriptional Activation - drug effects Vertebrates: endocrinology |
title | MAPK Phosphatase-1 (MKP-1) Expression Is Up-Regulated by hCG/cAMP and Modulates Steroidogenesis in MA-10 Leydig Cells |
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