Evidence map›Paper›PMID 9600917›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1998

Enhancing leptin response by preventing SH2-containing phosphatase 2 interaction with Ob receptor.

L R Carpenter, T J Farruggella, A Symes, M L Karow, G D Yancopoulos, N Stahl

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
4.4field-weighted citation impact, top 4% 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

47 citing papers in PubMed, 177 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Leptin Receptor Compound Heterozygosity in Humans and Animal Models.International journal of molecular sciences · 2021
    Review
  7. Role of SOCS3 in POMC neurons in metabolic and cardiovascular regulation.American journal of physiology. Regulatory, integrative and comparative physiology · 2019
    Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. The Leptin Receptor Complex: Heavier Than Expected?Frontiers in endocrinology · 2017
    Review
  15. The role of leptin in health and disease.Temperature (Austin, Tex.) · 2017
    Review
  16. Review
  17. Article
  18. Review
  19. Protein tyrosine phosphatase-1B contributes to LPS-induced leptin resistance in male rats.American journal of physiology. Endocrinology and metabolism · 2015
    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

6 authors at 2 institutions in 1 country.

L R CarpenterRegeneron Pharmaceuticals, Inc., 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA.
T J Farruggella
A Symes
M L Karow
G D Yancopoulos
N Stahl
Regeneron (United States) · USUniformed Services University of the Health Sciences · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Leptin is an adipocyte-derived cytokine that regulates food intake and body weight via interaction with its Ob receptor (ObR). Serum leptin levels are chronically elevated in obese humans, suggesting that obesity may be associated with leptin resistance and the inability to generate an adequate ObR response. Evidence suggests that transcriptional activation of target genes by STAT3 (signal transducer and activator of transcription) in the hypothalamus is a critical pathway that mediates leptin's action. Herein we report that activation of ObR induces the tyrosine phosphorylation of the tyrosine phosphatase SH2-containing phosphatase 2 (SHP-2) and demonstrate that Tyr986 within the ObR cytoplasmic domain is essential to mediate phosphorylation of SHP-2 and binding of SHP-2 to ObR. Surprisingly, mutation of Tyr986 to Phe, which abrogates SHP-2 phosphorylation and binding to the receptor, dramatically increases gene induction mediated by STAT3. Our findings indicate that SHP-2 is a negative regulator of STAT3-mediated gene induction after activation of ObR and raise the possibility that blocking the interaction of SHP-2 with ObR could overcome leptin resistance by boosting leptin's weight-reducing effects in obese individuals.

Indexed as

Receptors, Cell SurfaceSignal TransductionAnimalsCarrier ProteinsCOS CellsDNA-Binding ProteinsHumansIntracellular Signaling Peptides and ProteinsLeptinMutationObesityPhosphorylationProtein Phosphatase 2ProteinsProtein Tyrosine Phosphatase, Non-Receptor Type 11Protein Tyrosine Phosphatase, Non-Receptor Type 6Carrier ProteinsDNA-Binding ProteinsIntracellular Signaling Peptides and ProteinsLEPR protein, humanLeptinProtein Phosphatase 2ProteinsProtein Tyrosine Phosphatase, Non-Receptor Type 11Protein Tyrosine Phosphatase, Non-Receptor Type 6Protein Tyrosine PhosphatasesPTPN11 protein, humanPTPN6 protein, humanReceptors, Cell SurfaceReceptors, CytokineReceptors, LeptinSH2 Domain-Containing Protein Tyrosine PhosphatasesSTAT3 protein, humanSTAT3 Transcription FactorTrans-Activators

Identifiers

PMID9600917
PMCPMC27585
OpenAlexW2052743140

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.