PTP1B Deficiency Exacerbates Inflammation and Accelerates Leukocyte Trafficking In Vivo

No abstract is available for this paper.

• Publication year

  2012

• Venue

  Journal of Immunology

• Publication date

  2012-01-15

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.4049/jimmunol.1004108PMID 22156494PMCID PMC3253258
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• The fifth author's name was omitted from the article. The corrected author and affiliation lines are shown below.

  2013cited by this paper
• Correction: PTP1B Deficiency Exacerbates Inflammation and Accelerates Leukocyte Trafficking In Vivo

  2013cited by this paper
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• Corrections

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• Regulation of Insulin-Like Growth Factor Type I (IGF-I) Receptor Kinase Activity by Protein Tyrosine Phosphatase 1B (PTP-1B) and Enhanced IGF-I-Mediated Suppression of Apoptosis and Motility in PTP-1B-Deficient Fibroblasts

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• Eotaxin (CCL11) and Eotaxin-2 (CCL24) Induce Recruitment of Eosinophils, Basophils, Neutrophils, and Macrophages As Well As Features of Early- and Late-Phase Allergic Reactions Following Cutaneous Injection in Human Atopic and Nonatopic Volunteers1

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• A variation in 3' UTR of hPTP1B increases specific gene expression and associates with insulin resistance.

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• TYK2 and JAK2 Are Substrates of Protein-tyrosine Phosphatase 1B*

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• Immunotherapeutic implications of negative regulation by protein tyrosine phosphatases in T cells: the emerging cases of PTP1B and TCPTP

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• Recent Developments in the Role of Protein Tyrosine Phosphatase 1B (PTP1B) as a Regulator of Immune Cell Signalling in Health and Disease

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• The combination of a PTP1B inhibitor, TNFR2 blocker, and PD‑1 antibody suppresses the progression of non‑small cell lung cancer tumors by enhancing immunocompetence

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• Endothelial PTP1B Deletion Promotes VWF Exocytosis and Venous Thromboinflammation

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