• 제목/요약/키워드: Ras/MAPK

검색결과 46건 처리시간 0.029초

RAS SIGNALING IN INVASION AND MOTILITY OF MCF10A HUMAN BREAST EPITHELIAL CELLS

  • Kim, Mi-Sung;Lee, Eun-Jung;Shin, Il-Chung;Ahn, Seong-Min;Hyun Song;Kim, Hyeong-Reh-Choi;Aree Moon
    • 한국독성학회:학술대회논문집
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    • 한국독성학회 2002년도 Current Trends in Toxicological Sciences
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    • pp.76-77
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    • 2002

  • Ras expression has been suggested as a marker for tumor aggressiveness of breast cancer including the degrees of invasion and tumor recurrence. Expression of H-, K-, and N-ras is regulated in a tissue-specific manner and during development, indicating that ras proteins may have different cellular functions.(omitted)

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Induction of MAP kinase phosphatase 3 through Erk/MAP kinase activation in three oncogenic Ras (H-, K- and N-Ras)-expressing NIH/3T3 mouse embryonic fibroblast cell lines

  • Koo, JaeHyung;Wang, Sen;Kang, NaNa;Hur, Sun Jin;Bahk, Young Yil
    • BMB Reports
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    • 제49권7호
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    • pp.370-375
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    • 2016

  • Ras oncoproteins are small molecular weight GTPases known for their involvement in oncogenesis, which operate in a complex signaling network with multiple effectors. Approximately 25% of human tumors possess mutations in a member of this family. The Raf1/MEK/Erk1/2 pathway is one of the most intensively studied signaling mechanisms. Different levels of regulation account for the inactivation of MAP kinases by MAPK phosphatases in a cell type- and stimuli-dependent manner. In the present study, using three inducible Ras-expressing NIH/3T3 cell lines, we demonstrated that MKP3 upregulation requires the activation of the Erk1/2 pathway, which correlates with the shutdown of this pathway. We also demonstrated, by applying pharmacological inhibitors and effector mutants of Ras, that induction of MKP3 at the protein level is positively regulated by the oncogenic Ras/Raf/MEK/Erk1/2 signaling pathway.

  • https://doi.org/10.5483/BMBRep.2016.49.7.256 인용 PDF KSCI KPUBS HTML

Roles of PI3K and Rac Pathways in H-ras Induced Invasion and Motility

  • Ilchung Shin;Kim, Seonhoe;Aree Moon
    • 한국독성학회:학술대회논문집
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    • 한국독성학회 2003년도 추계학술대회
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    • pp.144-144
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    • 2003

  • Phosphatidylinositol 3-kinase (PI3K) and Rac play important roles that regulate cellular functions including cell survival and .migration. In the present study, we investigated the functional roles of PI3K and Rac1 pathways in H-ras-induced invasive phenotype and motility of MCF10A cells.(omitted)

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Differential Activation of Ras/Raf/MAPK Pathway between Heart and Cerebral Artery in Isoproterenol-induced Cardiac Hypertrophy

  • Kim, Hyun-Ju;Kim, Na-Ri;Joo, Hyun;Youm, Jae-Boum;Park, Won-Sun;Warda, Mohamed;Kang, Sung-Hyun;Thu, Vu-Thi;Khoa, Tran-Minh;Han, Jin
    • The Korean Journal of Physiology and Pharmacology
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    • 제9권5호
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    • pp.299-304
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    • 2005

  • Cardiac hypertrophy contributes an increased risk to major cerebrovascular events. However, the molecular mechanisms underlying cerebrovascular dysfunction during cardiac hypertrophy have not yet been characterized. In the present study, we examined the molecular mechanism of isoproterenol (ISO)-evoked activation of Ras/Raf/MAPK pathways as well as PKA activity in cerebral artery of rabbits, and we also studied whether the activations of these signaling pathways were altered in cerebral artery, during ISO-induced cardiac hypertrophy compared to heart itself. The results show that the mRNA level of c-fos (not c-jun and c-myc) in heart and these genes in cerebral artery were considerably increased during cardiac hypertrophy. These results that the PKA activity and activations of Ras/Raf/ERK cascade as well as c-fos expression in rabbit heart during cardiac hypertrophy were consistent with previous reports. Interestingly, however, we also showed a novel finding that the decreased PKA activity might have differential effects on Ras and Raf expression in cerebral artery during cardiac hypertrophy. In conclusion, there are differences in molecular mechanisms between heart and cerebral artery during cardiac hypertrophy when stimulated with β2 adrenoreceptor (AR), suggesting a possible mechanism underlying cerebrovascular dysfunction during cardiac hypertrophy.

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Overexpression of GAP Causes the Delay of NGF-induced Neuronal Differentiation and the Inhibition of Tyrosine Phosphorylation of SNT in PC12 Cells

  • Yang, Sung-Il;Kaplan, David
    • BMB Reports
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    • 제28권4호
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    • pp.316-322
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    • 1995

  • The GTPase activating protein (GAP) can function both as a negative regulator and an effector of $p21^{ras}$. Overexpression of GAP in NIH-3T3 cells has been shown to inhibit transformation by ms or src. To investigate the function of GAP in a differentiative system, we overexpressed this protein in the nerve growth factor (NGF)-responsive PC12 cell line. Two-fold overexpression of GAP caused a delay of several days in the onset of NGF- but not FGF-induced neuronal differentiation of PC12 cells. However, the NGF-induced activation or tyrosine phosphorylation of upstream (Trk, PLC-${\gamma}1$, SHC) and downstream (B-Raf and $p44^{mapk/erk1}$) components of $p21^{ras}$, signalling cascade was not altered by GAP overexpression. Therefore, the change of phenotype induced by GAP was probably not due to GAP functioning as a negative regulator of $p21^{ras}$. Rather, we found that NGF-induced tyrosine phosphorylation of SNT, a specific target of neurotrophin-induced tyrosine kinase activity, was inhibited by GAP overexpression. SNT is thought to function upstream or independent of $p21^{ras}$. Thus in PC12 cells, overexpressed GAP may control the rate of neuronal differentiation through a pathway involving SNT rather than the $p21^{ras}$ signalling pathway.

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