Evidence map›Paper›PMID 11516103›Full record

ArticleLeukemia2001

Role of the tyrosine phosphatase SHP-1 in K562 cell differentiation.

B Bruecher-Encke, J D Griffin, B G Neel, U Lorenz

Abstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2001. 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
0.8field-weighted citation impact, top 28% 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, 58 citations in OpenAlex.

  1. Epigenetics in psoriasis: perspective of DNA methylation.Molecular genetics and genomics : MGG · 2021
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Resveratrol induces human K562 cell apoptosis, erythroid differentiation, and autophagy.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014
    Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Src kinase signaling in leukaemia.The international journal of biochemistry & cell biology · 2007
    Review
  17. Article
  18. Role of protein tyrosine phosphatases in cancer.Progress in nucleic acid research and molecular biology · 2006
    Review
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

4 authors at 3 institutions in 1 country.

B Bruecher-EnckeDepartment of Medicine, Beth Israel-Deaconess Medical Center, Boston, MA, USA.
J D Griffin
B G Neel
U Lorenz
Beth Israel Deaconess Medical Center · USHarvard University · USUniversity of Virginia · US

Funding

SIGNAL TRANSDUCTION PATHWAYS IN STABLE PHASE CHRONIC MYELOID LEUKEMIA CELLSP01DK050654 · NIDDK · DANA-FARBER CANCER INSTITUTE · PI D'ANDREA, ALAN DAVID · 1996 to 2006
$10.3M
NIDDK NIH HHS P01 DK50654
6 · The paper itself

Abstract

The erythro-megakaryoblastic leukemia cell line K562 undergoes erythroid or myeloid differentiation in response to treatment with various inducing agents. We observed that expression of the SH2-containing protein tyrosine phosphatase SHP-1 was induced upon exposure of K562 cells to differentiating agents. Under the same conditions, expression of SHP-2, a close relative of SHP-1, and the more distantly related PTP-1 B remained unchanged. Induction of SHP-1 expression correlates with dephosphorylation of a specific and limited set of tyrosyl phosphoproteins, suggesting that dephosphorylation of these proteins may be important for the differentiation process. Importantly, expression of exogenous SHP-1 inhibits K562 proliferation and alters the adhesion properties of these cells, indicating a more differentiated phenotype. Moreover, SHP-1 is found in a complex with both p210 Bcr-Abl and p190 Bcr-Abl, suggesting that it may regulate Bcr-Abl or Bcr-Abl-associated phosphotyrosyl proteins. Our results indicate that induction of SHP-1 expression is important for K562 differentiation in response to various inducers and raise the possibility that functional inactivation of SHP-1 may play a role in progression to blast crisis in chronic myelogenous leukemia.

Indexed as

Cell AdhesionCell DifferentiationCell DivisionElectrophoresis, Polyacrylamide GelEnzyme InductionFusion Proteins, bcr-ablHL-60 CellsHumansIntracellular Signaling Peptides and ProteinsK562 CellsLeukemia, Myelogenous, Chronic, BCR-ABL PositivePhenotypeProtein Tyrosine Phosphatase, Non-Receptor Type 6Protein Tyrosine Phosphatasessrc Homology DomainsFusion Proteins, bcr-ablIntracellular Signaling Peptides and ProteinsProtein Tyrosine Phosphatase, Non-Receptor Type 6Protein Tyrosine PhosphatasesPTPN6 protein, human

Identifiers

PMID11516103
OpenAlexW2324997809

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.