Ca(2+)/calmodulin-dependent protein kinase (CaM-kinase) inhibitor KN-62 suppresses the activity of mitogen-activated protein kinase (MAPK), c-myc activation and human keratinocyte proliferation.

Praskova M; Kalenderova S; Miteva L; Poumay Y; Mitev V

首页> 外文期刊>Archives of dermatological research. >Ca(2+)/calmodulin-dependent protein kinase (CaM-kinase) inhibitor KN-62 suppresses the activity of mitogen-activated protein kinase (MAPK), c-myc activation and human keratinocyte proliferation.

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Ca(2+)/calmodulin-dependent protein kinase (CaM-kinase) inhibitor KN-62 suppresses the activity of mitogen-activated protein kinase (MAPK), c-myc activation and human keratinocyte proliferation.

机译：Ca（2 +）/钙调蛋白依赖性蛋白激酶（CaM激酶）抑制剂KN-62抑制有丝分裂原激活的蛋白激酶（MAPK），c-myc激活和人类角质形成细胞增殖的活性。

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Autocrine growth of human epidermal keratinocytes can be maintained in subconfluent cell cultures in the absence of exogenous growth factors. We used this culture model to investigate the interactions between the mitogen-activated protein kinase (MAPK) pathway and Ca(2+)/calmodulin-dependent protein kinases (CaM-kinases) in autocrine keratinocyte proliferation. We have previously demonstrated that MAPK and protein kinase C (PKC) are both involved in keratinocyte proliferation in a complex set of interactions. Treatment of keratinocytes with PD98059, a potent inhibitor of MAPK kinase, inhibited the MAPK pathway, c-myc activation and autocrine keratinocyte proliferation. Application of the CaM-kinase inhibitor KN-62 also led to a strong inhibition of MAPK/c-myc activation and autocrine keratinocyte proliferation. Other inhibitors, such as wortmannin (selective and potent inhibitor of phosphatidylinositol 3-kinase) and AG 490 (JAK2 inhibitor) had weak effects on autocrine keratinocyte proliferation, MAPK and c-myc activation. Our results clearly demonstrate a crosstalk between CaM-kinase/MAPK pathways in transducing keratinocyte proliferation stimuli.

机译：人表皮角质形成细胞的自分泌生长可以在没有外源生长因子的情况下在亚汇合细胞培养物中维持。我们使用这种培养模型来研究自分泌角质形成细胞增殖中丝裂原激活的蛋白激酶（MAPK）途径和Ca（2 +）/钙调蛋白依赖性蛋白激酶（CaM激酶）之间的相互作用。我们以前已经证明，MAPK和蛋白激酶C（PKC）都以复杂的相互作用集参与角质形成细胞的增殖。用PD98059（一种有效的MAPK激酶抑制剂）治疗角质形成细胞，可抑制MAPK途径，c-myc激活和自分泌角质形成细胞增殖。 CaM激酶抑制剂KN-62的应用也导致对MAPK / c-myc激活和自分泌角质形成细胞增殖的强烈抑制。其他抑制剂，如渥曼青霉素（磷脂酰肌醇3-激酶的选择性和有效抑制剂）和AG 490（JAK2抑制剂）对自分泌角质形成细胞增殖，MAPK和c-myc活化作用较弱。我们的结果清楚地证明了CaM激酶/ MAPK通路在转导角质形成细胞增殖刺激中的串扰。

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《Archives of dermatological research.》 |2002年第4期|共5页
作者
Praskova M; Kalenderova S; Miteva L; Poumay Y; Mitev V;
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正文语种 eng
中图分类皮肤病学与性病学;
关键词
Mitogen-Activated Protein Kinases; Keratinocytes; Phosphotransferases; 角蛋白细胞; 磷酸转移酶类;

机译：Mitogen-Activated Protein Kinases;Keratinocytes;Phosphotransferases;角蛋白细胞;磷酸转移酶类;

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1. Ca(2+)/calmodulin-dependent protein kinase (CaM-kinase) inhibitor KN-62 suppresses the activity of mitogen-activated protein kinase (MAPK), c-myc activation and human keratinocyte proliferation. [J] . Praskova M, Kalenderova S, Miteva L, Archives of dermatological research. . 2002,第4期

机译：Ca（2 +）/钙调蛋白依赖性蛋白激酶（CaM激酶）抑制剂KN-62抑制有丝分裂原激活的蛋白激酶（MAPK），c-myc激活和人类角质形成细胞增殖的活性。
2. Flavopiridol suppresses tumor necrosis factor-induced activation of activator protein-1, c-Jun N-terminal kinase, p38 mitogen-activated protein kinase (MAPK), p44/p42 MAPK, and Akt, inhibits expression of antiapoptotic gene products, and enhances apo [J] . Takada Y, Sethi G, Sung B, Molecular pharmacology. . 2008,第5期

机译：黄酮哌啶醇抑制肿瘤坏死因子诱导的活化蛋白1，c-Jun N端激酶，p38丝裂原活化蛋白激酶（MAPK），p44 / p42 MAPK和Akt的激活，抑制抗凋亡基因产物的表达，并增强apo
3. Dual role of protein kinase C on mitogen-activated protein kinase activation and human keratinocyte proliferation. [J] . Praskova M, Kalenderova S, Miteva L, Experimental dermatology . 2002,第4期

机译：蛋白激酶C对有丝分裂原激活的蛋白激酶激活和人类角质形成细胞增殖的双重作用。
4. Activation of Mitogen-activated Protein Kinases and Protein Kinase B/akt Signaling By Oxidative Stress in Vascular Smooth Muscle Cells: involvement in Vascular Pathophysiology [C] . Ashok K. Srivastava, Nihar R. Pandey, Antoine Blanc International Society for Heart Research.Congress . 2004

机译：血管平滑肌细胞氧化应激激活丝裂剂活化蛋白激酶和蛋白激酶B / Akt信号传导：血管病理生理学中的参与
5. Mitogen-activated protein kinase signaling alterations and functional consequences of arsenite and ultraviolet irradiation in human keratinocytes. [D] . Cooper, Karen L. 2007

机译：丝裂素活化的蛋白激酶信号转导以及人角质形成细胞中亚砷酸盐和紫外线的作用及其功能后果。
6. Re: Takada Y Sethi G Sung B and Aggarwal BB (2008) Flavopiridol suppresses tumor necrosis factor-induced activation of activator protein-1 c-Jun N-terminal kinase p38 mitogen-activated protein kinase (MAPK) p44/p42 MAPK and Akt inhibits expression of antiapoptotic gene products and enhances apoptosis through cytochrome c release and caspase activation in human myeloid cells Mol Pharmacol May 2008 73:1549–1557; doi:10.1124/mol.107.041350 [O] . -1

机译：回复：Takada YSethi GSung B和Aggarwal BB（2008）黄酮哌啶醇可抑制肿瘤坏死因子诱导的活化蛋白1c-Jun N端激酶p38丝裂原活化蛋白激酶（MAPK）p44活化/ p42 MAPK和Akt可以抑制抗凋亡基因产物的表达并通过细胞色素c释放和胱天蛋白酶在人骨髓细胞中的活化来增强细胞凋亡Mol Pharmacol2008年5月73：1549-1557； doi：10.1124 / mol.107.041350
7. Re: Takada Y, Sethi G, Sung B, and Aggarwal BB (2008) Flavopiridol suppresses tumor necrosis factor-induced activation of activator protein-1, c-Jun N-terminal kinase, p38 mitogen-activated protein kinase (MAPK), p44/p42 MAPK, and Akt, inhibits expression of antiapoptotic gene products, and enhances apoptosis through cytochrome c release and caspase activation in human myeloid cells Mol Pharmacol May 2008 73:1549–1557; doi:10.1124/mol.107.041350 [O] . 2016

机译：Re：Takada Y，Sethi G，Sung B和Aggarwal BB（2008）抑制肿瘤坏死因子诱导的活化剂蛋白-1，C-6末端激酶，P38丝裂原激活蛋白激酶（MAPK），P44 / p42 mapk和akt抑制抗凋亡基因产物的表达，并通过细胞色素C释放和Caspase活化在人骨髓细胞Mol Pharmacol 2008年5月73：1549-1557中增强细胞凋亡。 DOI：10.1124 / mol.107.041350

Ca(2+)/calmodulin-dependent protein kinase (CaM-kinase) inhibitor KN-62 suppresses the activity of mitogen-activated protein kinase (MAPK), c-myc activation and human keratinocyte proliferation.

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