Evidence map›Paper›PMID 10445846›Full record

ArticleOncogene1999

Cellular functions of TC10, a Rho family GTPase: regulation of morphology, signal transduction and cell growth.

G A Murphy, P A Solski, S A Jillian, P Pérez de la Ossa, P D'Eustachio, C J Der, M G Rush

Abstract readComparative Study
PubMed Publisher
In one paragraph

Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.2field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

33 citing papers in PubMed, 107 citations in OpenAlex.

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  19. Collybistin activation by GTP-TC10 enhances postsynaptic gephyrin clustering and hippocampal GABAergic neurotransmission.Proceedings of the National Academy of Sciences of the United States of America · 2013
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

G A MurphyDepartment of Biochemistry, New York University Medical Center, New York 10016, USA.
P A Solski
S A Jillian
P Pérez de la Ossa
P D'Eustachio
C J Der
M G Rush
New York University · USColumbia University Irving Medical Center · USUNC Lineberger Comprehensive Cancer Center

Funding

BIOLOGICAL ACTIVITY OF RAS ONCOGENESR01CA042978 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DER, CHANNING J. · 1986 to 2017
$5.9M
RHO FAMILY PROTEINS AND MALIGNANT TRANSFORMATIONR01CA063071 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DER, CHANNING J · 1994 to 2007
$2.0M
FUNCTION OF RAS ONCOGENE PROTEIN RELATED RAB PROTEINSR01CA055008 · NCI · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI DER, CHANNING J · 1991 to 1995
–
NCI NIH HHS CA42978NCI NIH HHS CA55008NCI NIH HHS CA63071
6 · The paper itself

Abstract

The small Ras-related GTPase, TC10, has been classified on the basis of sequence homology to be a member of the Rho family. This family, which includes the Rho, Rac and CDC42 subfamilies, has been shown to regulate a variety of apparently diverse cellular processes such as actin cytoskeletal organization, mitogen-activated protein kinase (MAPK) cascades, cell cycle progression and transformation. In order to begin a study of TC10 biological function, we expressed wild type and various mutant forms of this protein in mammalian cells and investigated both the intracellular localization of the expressed proteins and their abilities to stimulate known Rho family-associated processes. Wild type TC10 was located predominantly in the cell membrane (apparently in the same regions as actin filaments), GTPase defective (75L) and GTP-binding defective (31N) mutants were located predominantly in cytoplasmic perinuclear regions, and a deletion mutant lacking the carboxyl terminal residues required for post-translational prenylation was located predominantly in the nucleus. The GTPase defective (constitutively active) TC10 mutant: (1) stimulated the formation of long filopodia; (2) activated c-Jun amino terminal kinase (JNK); (3) activated serum response factor (SRF)-dependent transcription; (4) activated NF-kappaB-dependent transcription; and (5) synergized with an activated Raf-kinase (Raf-CAAX) to transform NIH3T3 cells. In addition, wild type TC10 function is required for full H-Ras transforming potential. We demonstrate that an intact effector domain and carboxyl terminal prenylation signal are required for proper TC10 function and that TC10 signals to at least two separable downstream target pathways. In addition, TC10 interacted with the actin-binding and filament-forming protein, profilin, in both a two-hybrid cDNA library screen, and an in vitro binding assay. Taken together, these data support a classification of TC10 as a member of the Rho family, and in particular, suggest that TC10 functions to regulate cellular signaling to the actin cytoskeleton and processes associated with cell growth.

Indexed as

Contractile ProteinsMitogen-Activated Protein Kinasesrho GTP-Binding Proteins3T3 CellsAmino Acid SequenceAnimalsCalcium-Calmodulin-Dependent Protein Kinasescdc42 GTP-Binding ProteinCell Cycle ProteinsCell DivisionCell SizeCell Transformation, NeoplasticChlorocebus aethiopsCOS CellsDNA-Binding ProteinsDNA, ComplementaryCalcium-Calmodulin-Dependent Protein Kinasescdc42 GTP-Binding ProteinCell Cycle ProteinsContractile ProteinsDNA-Binding ProteinsDNA, ComplementaryGTP-Binding ProteinsGTP PhosphohydrolasesJNK Mitogen-Activated Protein KinasesMicrofilament ProteinsMitogen-Activated Protein KinasesNF-kappa BNuclear ProteinsPfn1 protein, mouseProfilinsrac GTP-Binding ProteinsRecombinant Fusion ProteinsrhoA GTP-Binding Proteinrho GTP-Binding ProteinsRhoq protein, mouseSerum Response Factor

Identifiers

PMID10445846
OpenAlexW2071839580

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.