Evidence map›Paper›PMID 16024808›Full record

ArticleMolecular and cellular biology2005

Repression of c-kit and its downstream substrates by GATA-1 inhibits cell proliferation during erythroid maturation.

Veerendra Munugalavadla, Louis C Dore, Bai Lin Tan, Li Hong, Melanie Vishnu, Mitchell J Weiss, Reuben Kapur

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 1 pooled it
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

67 citing papers in PubMed, 1 synthesis or guideline pooled it, 105 citations in OpenAlex.

  1. Pooled it
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  14. Combination of Luteolin and Solifenacin Improves Urinary Dysfunction Induced by Diabetic Cystopathy in Rats.Medical science monitor : international medical journal of experimental and clinical research · 2018
    Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Derepression of the DNA Methylation Machinery of theMolecular and cellular biology · 2017
    Article

7 more citing papers are in PubMed but not listed here.

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.

Veerendra MunugalavadlaHerman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Cancer Research Institute, 1044 W. Walnut Street, Room 425, Indianapolis, IN 46202, USA. vmunugal@iupui.edu
Louis C Dore
Bai Lin Tan
Li Hong
Melanie Vishnu
Mitchell J Weiss
Reuben Kapur
University School · USChildren's Hospital of Philadelphia · USCalifornia University of Pennsylvania · US

Funding

Trim58 and the Ubiquitin Proteasome System in Erythro-megakaryopoiesisR01DK061692 · NIDDK · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI WEISS, MITCHELL J · 2002 to 2018
$5.6M
Mechanisms of adhesion and growth control in stem cellsR01HL075816 · NHLBI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI KAPUR, REUBEN · 2004 to 2010
$2.3M
Antiproliferative actions of GATA-1 during hematopoiesisR01DK064037 · NIDDK · CHILDREN'S HOSP OF PHILADELPHIA · PI WEISS, MITCHELL J · 2004 to 2006
$741k
NHLBI NIH HHS R01 HL075816NIDDK NIH HHS R01 DK064037
6 · The paper itself

Abstract

Stem cell factor (SCF), erythropoietin (Epo), and GATA-1 play an essential role(s) in erythroid development. We examined how these proteins interact functionally in G1E cells, a GATA-1(-) erythroblast line that proliferates in an SCF-dependent fashion and, upon restoration of GATA-1 function, undergoes GATA-1 proliferation arrest and Epo-dependent terminal maturation. We show that SCF-induced cell cycle progression is mediated via activation of the Src kinase/c-Myc pathway. Restoration of GATA-1 activity induced G1 cell cycle arrest coincident with repression of c-Kit and its downstream effectors Vav1, Rac1, and Akt. Sustained expression of each of these individual signaling components inhibited GATA-1-induced cell cycle arrest to various degrees but had no effects on the expression of GATA-1-regulated erythroid maturation markers. Chromatin immunoprecipitation analysis revealed that GATA-1 occupies a defined Kit gene regulatory element in vivo, suggesting a direct mechanism for gene repression. Hence, in addition to its well-established function as an activator of erythroid genes, GATA-1 also participates in a distinct genetic program that inhibits cell proliferation by repressing the expression of multiple components of the c-Kit signaling axis. Our findings reveal a novel aspect of molecular cross talk between essential transcriptional and cytokine signaling components of hematopoietic development.

Indexed as

Cell ProliferationAnimalsApoptosisCell DifferentiationCell Line, TransformedClone CellsDNA-Binding ProteinsErythroid CellsErythroid-Specific DNA-Binding FactorsErythropoietinGATA1 Transcription FactorGene Expression RegulationGrowth InhibitorsMiceProto-Oncogene Proteins c-kitRepressor ProteinsDNA-Binding ProteinsErythroid-Specific DNA-Binding FactorsErythropoietinGata1 protein, mouseGATA1 Transcription FactorGrowth InhibitorsProto-Oncogene Proteins c-kitRepressor Proteinssrc-Family KinasesStem Cell FactorTranscription Factors

Identifiers

PMID16024808
PMCPMC1190349
OpenAlexW2108718984

What Socratic 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 Socratic graph.