Evidence map›Paper›PMID 27216862›Full record

ReviewImmunologic research2016

Protein tyrosine phosphatase SHP-1: resurgence as new drug target for human autoimmune disorders.

Yadhu Sharma, Samina Bashir, Puja Bhardwaj, Altaf Ahmad, Farah Khan

Abstract readReview
PubMed Publisher
In one paragraph

Review in Immunologic research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

19 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Loss of SHP-1 in CD11cFrontiers in immunology · 2026
    Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. A signalling cascade involving receptor-activated phospholipase ACell communication and signaling : CCS · 2019
    Article
  15. EnterohemorrhagicEmerging microbes & infections · 2019
    Article
  16. Article
  17. Shp1 function in myeloid cells.Journal of leukocyte biology · 2017
    Review
  18. Article
  19. 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

5 authors at 2 institutions in 1 country.

Yadhu SharmaDepartment of Biochemistry, Faculty of Science, Jamia Hamdard, New Delhi, 110062, India.
Samina BashirDepartment of Biochemistry, Faculty of Science, Jamia Hamdard, New Delhi, 110062, India.
Puja BhardwajDepartment of Biochemistry, Faculty of Science, Jamia Hamdard, New Delhi, 110062, India.
Altaf AhmadDepartment of Botany, Aligarh Muslim University, Aligarh, Uttar Pradesh, 202002, India.
Farah KhanDepartment of Biochemistry, Faculty of Science, Jamia Hamdard, New Delhi, 110062, India. farahkhan3@gmail.com.
Jamia Hamdard · INAligarh Muslim University · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recognition of self-antigen and its destruction by the immune system is the hallmark of autoimmune diseases. During the developmental stages, immune cells are introduced to the self-antigen, for which tolerance develops. The inflammatory insults that break the immune tolerance provoke immune system against self-antigen, progressively leading to autoimmune diseases. SH2 domain containing protein tyrosine phosphatase (PTP), SHP-1, was identified as hematopoietic cell-specific PTP that regulates immune function from developing immune tolerance to mediating cell signaling post-immunoreceptor activation. The extensive research on SHP-1-deficient mice elucidated the diversified role of SHP-1 in immune regulation, and inflammatory process and related disorders such as cancer, autoimmunity, and neurodegenerative diseases. The present review focalizes upon the implication of SHP-1 in the pathogenesis of autoimmune disorders, such as allergic asthma, neutrophilic dermatosis, atopic dermatitis, rheumatoid arthritis, and multiple sclerosis, so as to lay the background in pursuance of developing therapeutic strategies targeting SHP-1. Also, new SHP-1 molecular targets have been suggested like SIRP-α, PIPKIγ, and RIP-1 that may prove to be the focal point for the development of therapeutic strategies.

Indexed as

AnimalsAntigens, DifferentiationAutoantigensAutoimmune DiseasesHumansImmune ToleranceIntracellular Signaling Peptides and ProteinsMiceMice, KnockoutMolecular Targeted TherapyPhosphotransferases (Alcohol Group Acceptor)Protein Tyrosine Phosphatase, Non-Receptor Type 6Receptors, ImmunologicSignal TransductionT-Lymphocytes1-phosphatidylinositol-4-phosphate 5-kinaseAntigens, DifferentiationAutoantigensIntracellular Signaling Peptides and ProteinsPAK1IP1 protein, humanPhosphotransferases (Alcohol Group Acceptor)Protein Tyrosine Phosphatase, Non-Receptor Type 6Receptors, ImmunologicSIRPA protein, humanAutoimmune diseasesInflammationMotheaten miceSHP-1T cellViable motheaten mice

Identifiers

PMID27216862
OpenAlexW2398961842

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.