NDLI: Angiotensin II stimulates ERK via two pathways in epithelial cells: protein kinase C suppresses a G-protein coupled receptor-EGF receptor transactivation pathway.

Please wait, while we are loading the content...

Angiotensin II stimulates ERK via two pathways in epithelial cells: protein kinase C suppresses a G-protein coupled receptor-EGF receptor transactivation pathway.

A unique insert in the linker domain of Syk is necessary for its function in immunoreceptor signalling.

Mammalian thioredoxin is a direct inhibitor of apoptosis signal-regulating kinase (ASK) 1.

Modulation of HIV-1 infectivity by MAPK, a virion-associated kinase.

A mitogen-activated protein (MAP) kinase homologue of Leishmania mexicana is essential for parasite survival in the infected host.

The redox-regulated SoxR protein acts from a single DNA site as a repressor and an allosteric activator.

Selection in vitro of novel ribozymes from a partially randomized U2 and U6 snRNA library.

Dbp5p, a cytosolic RNA helicase, is required for poly(A)+ RNA export.

Dbp5p/Rat8p is a yeast nuclear pore-associated DEAD-box protein essential for RNA export.

hMSH2 and hMSH6 play distinct roles in mismatch binding and contribute differently to the ATPase activity of hMutSalpha.

RAD9 and RAD24 define two additive, interacting branches of the DNA damage checkpoint pathway in budding yeast normally required for Rad53 modification and activation.

Efficient HIV-1 replication can occur in the absence of the viral matrix protein.

Hydration and recognition of methylated CpG steps in DNA.

Year: 1998, Volume: 17, Issue: 8

Year: 1998, Volume: 17, Issue: 7

Year: 1998, Volume: 17, Issue: 6

Year: 1998, Volume: 17, Issue: 5

Year: 1998, Volume: 17, Issue: 4

Year: 1998, Volume: 17, Issue: 3

Year: 1998, Volume: 17, Issue: 2

Year: 1998, Volume: 17, Issue: 1

Year: 1997, Volume: 16

Year: 1996, Volume: 15

Year: 1995, Volume: 14

Year: 1994, Volume: 13

Year: 1993, Volume: 12

Year: 1992, Volume: 11

Year: 1991, Volume: 10

Year: 1990, Volume: 9

Year: 1989, Volume: 8

Year: 1988, Volume: 7

Year: 1987, Volume: 6

Year: 1986, Volume: 5

Year: 1985, Volume: 4

Year: 1984, Volume: 3

Year: 1983, Volume: 2

Year: 1982, Volume: 1

Angiotensin II stimulates ERK via two pathways in epithelial cells: protein kinase C suppresses a G-protein coupled receptor-EGF receptor transactivation pathway.

Content Provider	PubMed Central
Author	Lee, J. W. Graves, L. M. Earp, H. S. Li, X.
Abstract	In GN4 rat liver epithelial cells, angiotensin II (Ang II) produces intracellular calcium and protein kinase C (PKC) signals and stimulates ERK and JNK activity. JNK activation appears to be mediated by a calcium-dependent tyrosine kinase (CADTK). To define the ERK pathway, we established GN4 cells expressing an inhibitory Ras(N17). Induction of Ras(N17) blocked EGF- but not Ang II- or phorbol ester (TPA)-dependent ERK activation. In control cells, Ang II and TPA produced minimal increases in Ras-GTP level and Raf kinase activity. PKC depletion by chronic TPA exposure abolished TPA-dependent ERK activation but failed to diminish the effect of Ang II. In PKC-depleted cells, Ang II increased Ras-GTP level and activated Raf and ERK in a Ras-dependent manner. In PKC depleted cells, Ang II stimulated Shc and Cbl tyrosine phosphorylation, suggesting that without PKC, Ang II activates another tyrosine kinase. PKC-depletion did not alter Ang II-dependent tyrosine phosphorylation or activity of p125(FAK), CADTK, Fyn or Src, but PKC depletion or incubation with GF109203X resulted in Ang II-dependent EGF receptor tyrosine phosphorylation. In PKC-depleted cells, EGF receptor-specific tyrosine kinase inhibitors blocked Ang II-dependent EGF receptor and Cbl tyrosine phosphorylation, and ERK activation. In summary, Ang II can activate ERK via two pathways; the latent EGF receptor, Ras-dependent pathway is equipotent to the Ras-independent pathway, but is masked by PKC action. The prominence of this G-protein coupled receptor to EGF receptor pathway may vary between cell types depending upon modifiers such as PKC.
Related Links	http://dx.doi.org/10.1093/emboj/17.9.2574
Ending Page	2583
Page Count	10
Starting Page	2574
File Format	PDF
ISSN	14602075
e-ISSN	14602075
Journal	The EMBO Journal
Issue Number	9
Volume Number	17
Language	English
Publisher Date	1998-05-01
Access Restriction	Open
Subject Keyword	Biochemistry, Genetics and Molecular Biology(all) Immunology and Microbiology(all) Neuroscience(all) Molecular Biology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Neuroscience Immunology and Microbiology Medicine Molecular Biology

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Activation of MAPKs by Angiotensin II in Vascular Smooth Muscle Cells METALLOPROTEASE-DEPENDENT EGF RECEPTOR ACTIVATION IS REQUIRED FOR ACTIVATION OF ERK AND p38 MAPK BUT NOT FOR JNK

The heterotrimeric G q protein-coupled angiotensin II receptor activates p21 ras via the tyrosine kinase-Shc-Grb2-Sos pathway in cardiac myocytes.

Carbachol Stimulates Transactivation of Epidermal Growth Factor Receptor and Mitogen-activated Protein Kinase in T84Cells IMPLICATIONS FOR CARBACHOL-STIMULATED CHLORIDE SECRETION

Biphasic Regulation of Yes-associated Protein (YAP) Cellular Localization, Phosphorylation, and Activity by G Protein-coupled Receptor Agonists in Intestinal Epithelial Cells A NOVEL ROLE FOR PROTEIN KINASE D (PKD)

Epidermal Growth Factor (EGF) Receptor-dependent ERK Activation by G Protein-coupled Receptors A CO-CULTURE SYSTEM FOR IDENTIFYING INTERMEDIATES UPSTREAM AND DOWNSTREAM OF HEPARIN-BINDING EGF SHEDDING

Intracellular Signaling of Angiotensin II-induced p70 S6 Kinase Phosphorylation at Ser411 in Vascular Smooth Muscle Cells POSSIBLE REQUIREMENT OF EPIDERMAL GROWTH FACTOR RECEPTOR, RAS, EXTRACELLULAR SIGNAL-REGULATED KINASE, AND AKT

The Stability of the G Protein-coupled Receptor-β-Arrestin Interaction Determines the Mechanism and Functional Consequence of ERK Activation

β-arrestin- and c-Src-dependent degradation of G-protein-coupled receptor kinase 2

Rapid Transactivation of the Vascular Endothelial Growth Factor Receptor KDR/Flk-1 by the Bradykinin B2 Receptor Contributes to Endothelial Nitric-oxide Synthase Activation in Cardiac Capillary Endothelial Cells

Angiotensin II stimulates ERK via two pathways in epithelial cells: protein kinase C suppresses a G-protein coupled receptor-EGF receptor transactivation pathway.

Similar Documents

Activation of MAPKs by Angiotensin II in Vascular Smooth Muscle Cells METALLOPROTEASE-DEPENDENT EGF RECEPTOR ACTIVATION IS REQUIRED FOR ACTIVATION OF ERK AND p38 MAPK BUT NOT FOR JNK

The heterotrimeric G q protein-coupled angiotensin II receptor activates p21 ras via the tyrosine kinase-Shc-Grb2-Sos pathway in cardiac myocytes.

Carbachol Stimulates Transactivation of Epidermal Growth Factor Receptor and Mitogen-activated Protein Kinase in T84Cells IMPLICATIONS FOR CARBACHOL-STIMULATED CHLORIDE SECRETION

Biphasic Regulation of Yes-associated Protein (YAP) Cellular Localization, Phosphorylation, and Activity by G Protein-coupled Receptor Agonists in Intestinal Epithelial Cells A NOVEL ROLE FOR PROTEIN KINASE D (PKD)

Epidermal Growth Factor (EGF) Receptor-dependent ERK Activation by G Protein-coupled Receptors A CO-CULTURE SYSTEM FOR IDENTIFYING INTERMEDIATES UPSTREAM AND DOWNSTREAM OF HEPARIN-BINDING EGF SHEDDING

Intracellular Signaling of Angiotensin II-induced p70 S6 Kinase Phosphorylation at Ser411 in Vascular Smooth Muscle Cells POSSIBLE REQUIREMENT OF EPIDERMAL GROWTH FACTOR RECEPTOR, RAS, EXTRACELLULAR SIGNAL-REGULATED KINASE, AND AKT

The Stability of the G Protein-coupled Receptor-β-Arrestin Interaction Determines the Mechanism and Functional Consequence of ERK Activation

β-arrestin- and c-Src-dependent degradation of G-protein-coupled receptor kinase 2

Rapid Transactivation of the Vascular Endothelial Growth Factor Receptor KDR/Flk-1 by the Bradykinin B2 Receptor Contributes to Endothelial Nitric-oxide Synthase Activation in Cardiac Capillary Endothelial Cells

Angiotensin II stimulates ERK via two pathways in epithelial cells: protein kinase C suppresses a G-protein coupled receptor-EGF receptor transactivation pathway.