Evidence map›Paper›PMID 17959833›Full record

ArticleMolecular biology of the cell2008

Using Bcr-Abl to examine mechanisms by which abl kinase regulates morphogenesis in Drosophila.

Traci L Stevens, Edward M Rogers, Laura M Koontz, Donald T Fox, Catarina C F Homem, Stephanie H Nowotarski, Nicholas B Artabazon, Mark Peifer

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

18 citing papers in PubMed, 28 citations in OpenAlex.

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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

8 authors at 2 institutions in 1 country.

Traci L StevensDepartment of Biology and Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-3280, USA.
Edward M Rogers
Laura M Koontz
Donald T Fox
Catarina C F Homem
Stephanie H Nowotarski
Nicholas B Artabazon
Mark Peifer
Ashland (United States) · USUniversity of North Carolina at Chapel Hill · US

Funding

Integrated Training in Cancer Model SystemsT32CA009156 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DER, CHANNING J. · 1985 to 2020
$19.7M
Cell adhesion, signal transduction and cytoskeletal regulation in DrosophilaR01GM047857 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI PEIFER, MARK A. · 1992 to 2016
$5.2M
ADHERENS JUNCTIONS SIGNALING PATHWAYS IN DROSOPHILAF32GM020797 · NIGMS · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI JESSE, TRACI L · 2001 to 2003
$100k
NCI NIH HHS 5T3CA09156NCI NIH HHS T32 CA009156NIGMS NIH HHS 1F32GM20797NIGMS NIH HHS F32 GM020797NIGMS NIH HHS GM-47857NIGMS NIH HHS R01 GM047857
6 · The paper itself

Abstract

Signaling by the nonreceptor tyrosine kinase Abelson (Abl) plays key roles in normal development, whereas its inappropriate activation helps trigger the development of several forms of leukemia. Abl is best known for its roles in axon guidance, but Abl and its relatives also help regulate embryonic morphogenesis in epithelial tissues. Here, we explore the role of regulation of Abl kinase activity during development. We first compare the subcellular localization of Abl protein and of active Abl, by using a phosphospecific antibody, providing a catalog of places where Abl is activated. Next, we explore the consequences for morphogenesis of overexpressing wild-type Abl or expressing the activated form found in leukemia, Bcr-Abl. We find dose-dependent effects of elevating Abl activity on morphogenetic movements such as head involution and dorsal closure, on cell shape changes, on cell protrusive behavior, and on the organization of the actin cytoskeleton. Most of the effects of Abl activation parallel those caused by reduction in function of its target Enabled. Abl activation leads to changes in Enabled phosphorylation and localization, suggesting a mechanism of action. These data provide new insight into how regulated Abl activity helps direct normal development and into possible biological functions of Bcr-Abl.

Indexed as

MorphogenesisAnimalsCell ShapeDNA-Binding ProteinsDrosophila melanogasterDrosophila ProteinsEmbryo, NonmammalianEnzyme ActivationFemaleFusion Proteins, bcr-ablMalePhosphorylationProtein TransportProtein-Tyrosine KinasesPseudopodiarho GTP-Binding ProteinsAbl protein, DrosophilaDNA-Binding ProteinsDrosophila ProteinsENA-VASP proteinsFusion Proteins, bcr-ablProtein-Tyrosine Kinasesrho GTP-Binding Proteins

Identifiers

PMID17959833
PMCPMC2174184
OpenAlexW2152395437

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.