Evidence map›Paper›PMID 11313480›Full record

ArticleMolecular and cellular biology2001

Socs-1 inhibits TEL-JAK2-mediated transformation of hematopoietic cells through inhibition of JAK2 kinase activity and induction of proteasome-mediated degradation.

J Frantsve, J Schwaller, D W Sternberg, J Kutok, D G Gilliland

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
8.9field-weighted citation impact, top 1% 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

54 citing papers in PubMed, 171 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. SOCS1 and its Potential Clinical Role in Tumor.Pathology oncology research : POR · 2019
    Review
  11. Article
  12. Article
  13. Ubiquitin-mediated NFκB degradation pathway.Cellular & molecular immunology · 2015
    Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. SOCS proteins in development and disease.American journal of clinical and experimental immunology · 2013
    Article
  19. Article
  20. Article
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

5 authors at 1 institution in 1 country.

J FrantsveDivision of Hematology, Department of Medicine, Boston, Massachusetts 02115.
J Schwaller
D W Sternberg
J Kutok
D G Gilliland
Harvard University · US

Funding

TYROSINE KINASE ONCOGENESIS IN MYELOID LEUKEMIAP01CA066996 · NCI · DANA-FARBER CANCER INSTITUTE · PI Zuzana Tothova · 1996 to 2026
$52.5M
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
SIGNAL TRANSDUCTION BY TEL/TYROSINE KINASE FUSIONSK08CA082261 · NCI · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI STERNBERG, DAVID W · 1999 to 2003
$557k
NCI NIH HHS CA82261NCI NIH HHS K08 CA082261NCI NIH HHS P01 CA066996NCI NIH HHS P01 CA66996NIDDK NIH HHS P01 DK050654NIDDK NIH HHS P01 DK50654
6 · The paper itself

Abstract

TEL-JAK2 fusion proteins, which are a result of t(9;12)(p24;p13) translocations associated with human leukemia, activate Stat5 in vitro and in vivo and cause a myelo- and lymphoproliferative disease in a murine bone marrow transplant model. We report that Socs-1, a member of the SOCS family of endogenous inhibitors of JAKs and STATs, inhibits transformation of Ba/F3 cells by TEL-JAK2 but has no effect on Ba/F3 cells transformed by BCR-ABL, TEL-ABL, or TEL-platelet-derived growth factor receptor beta. TEL-JAK2, in addition to activating Stat5, associates with Shc and Grb2 and induces activation of Erk2, and expression of Socs-1 inhibits engagement of each of these signaling molecules. TEL-JAK2 kinase activity is inhibited by Socs-1, as assessed by in vitro kinase assays. In addition, Socs-1 induces proteasomal degradation of TEL-JAK2. Mutational analysis indicates that the SOCS box of Socs-1 is required for proteasomal degradation and for abrogation of growth of TEL-JAK2-transformed cells. Furthermore, murine bone marrow transplant assays demonstrate that expression of Socs-1 prolongs latency of TEL-JAK2-mediated disease in vivo. Collectively, these data indicate that Socs-1 inhibits TEL-JAK2 in vitro and in vivo through inhibition of kinase activity and induction of TEL-JAK2 protein degradation.

Indexed as

Proto-Oncogene ProteinsRepressor ProteinsAnimalsCarrier ProteinsCell LineCell Transformation, NeoplasticCysteine EndopeptidasesEnzyme ActivationETS Translocation Variant 6 ProteinHematopoietic Stem CellsJanus Kinase 2MiceMultienzyme ComplexesOncogene Proteins, FusionProteasome Endopeptidase ComplexProtein-Tyrosine KinasesCarrier ProteinsCysteine EndopeptidasesETS Translocation Variant 6 ProteinJAK2 protein, humanJak2 protein, mouseJanus Kinase 2Multienzyme ComplexesOncogene Proteins, FusionProteasome Endopeptidase ComplexProtein-Tyrosine KinasesProto-Oncogene ProteinsRepressor ProteinsSocs1 protein, mouseSuppressor of Cytokine Signaling 1 ProteinSuppressor of Cytokine Signaling ProteinsTEL-JAK2 fusion protein, humanTEL-JAK2 fusion protein, mouse

Identifiers

PMID11313480
PMCPMC100276
OpenAlexW2142574099

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.