The DOI matches its Crossref record; 76 of the 76 references it cites were found in a registry or an index.
Protein-tyrosine phosphatase 1B expression is induced by inflammation in vivo.
Open accessAbstract
Protein-tyrosine phosphatase 1B (PTP1B) is a major negative regulator of insulin and leptin sensitivity. PTP1B overexpression in adipose tissue and skeletal muscle of humans and rodents may contribute to insulin resistance and obesity. The mechanisms mediating PTP1B overexpression in obese and diabetic states have been unclear. We find that adipose tissue inflammation and the pro-inflammatory cytokine tumor necrosis factor alpha (TNFalpha) regulate PTP1B expression in vivo. High fat feeding of mice increased PTP1B expression 1.5- to 7-fold in adipose tissue, liver, skeletal muscle, and arcuate nucleus of hypothalamus. PTP1B overexpression in high fat-fed mice coincided with increased adipose tissue expression of the macrophage marker CD68 and TNFalpha, which is implicated in causing obesity-induced insulin resistance. TNFalpha increased PTP1B mRNA and protein levels by 2- to 5-fold in a dose- and time-dependent manner in adipocyte and hepatocyte cell lines. TNFalpha administration in mice increased PTP1B mRNA 1.4- to 4-fold in adipose tissue, liver, skeletal muscle, and hypothalamic arcuate nucleus and PTP1B protein 2-fold in liver. Actinomycin D treatment blocked, and high dose salicylate treatment inhibited by 80%, TNFalpha-induced PTP1B expression in adipocyte cell lines, suggesting TNFalpha may induce PTP1B transcription via nuclear factor kappaB (NFkappaB) activation. Chromatin immunoprecipitation from adipocyte cell lines and liver of mice demonstrated TNFalpha-induced recruitment of NFkappaB subunit p65 to the PTP1B promoter in vitro and in vivo. In mice with diet-induced obesity, TNFalpha deficiency also partly blocked PTP1B overexpression in adipose tissue. Our data suggest that PTP1B overexpression in multiple tissues in obesity is regulated by inflammation and that PTP1B may be a target of anti-inflammatory therapies.
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“Consistent with this, the cellular effects of leptin have been amplified in cells lacking either SOCS3 or PT1b, a phosphotyrosine phosphatase.”
From Leptin at 14 y of age: an ongoing story (2009) · cites this paper as [47]
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“Importantly, mice with haploinsufficiency for either of these genes are resistant to obesity, remain lean on a high-fat diet, and retain leptin sensitivity (46,47).”
From Leptin at 14 y of age: an ongoing story (2009) · cites this paper as [47]
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1 retracted
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Items 401–407 of 407
Xu, D., He, C., Lv, H., Weedor, J. G., Xing, Y., He, Z., Jing, P., Cui, W., Yang, X., Zhao, G., et al. (2026) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2026.106894
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BindingDB Entry 50018994: Characterization of Serrulatane Diterpenoids in
BindingDB (2024) · UC San Diego · doi:10.7270/q2dn4995
BindingDB (2019) · UC San Diego · doi:10.7270/q21j9d18
Metadata
- Authors
- Zabolotny, J. M., Kim, Y.-B., Welsh, L. A., Kershaw, E. E., Neel, B. G., & Kahn, B. B.
- Affiliations
- Beth Israel Deaconess Medical Center (US)
- Corresponding author
- Zabolotny, Janice M.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2008-05
- Volume
- 283
- Issue
- 21
- Pages
- 14230-14241
- ISSN
- 0021-9258 (ISSN-L)
- PMC
- PMC2386946
- OpenAlex
- W2120790798
- Cited by
- 404
- References
- 76
- Citations by year
- 2026: 5 · 2025: 12 · 2024: 17 · 2023: 17 · 2022: 22 · 2021: 24 · 2020: 21 · 2019: 25 · 2018: 15 · 2017: 20 · 2016: 25 · 2015: 30 · 2014: 26 · 2013: 33 · 2012: 47
- FWCI
- 8.92
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Diabetes Association
- National Institutes of Health (DK057521, DK046200)
- National Cancer Institute (R01CA049152)
- National Institute of Diabetes and Digestive and Kidney Diseases (P30DK057521, R21DK073530, K01DK062212, P30DK046200, R01DK060839, R01DK060838, K08DK065833)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Tyrosine Phosphatases
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Keywords
- PTP1B, adipose tissue inflammation, TNF-α, obesity, insulin resistance, leptin sensitivity, NF-κB, high-fat feeding, diet-induced obesity, CD68+ macrophages, hypothalamic arcuate nucleus, liver, skeletal muscle, anti-inflammatory therapy
- MeSH terms
- Animals, Animal Feed, Base Sequence, Cells, Cultured, Diabetes Mellitus, Inflammation, Insulin, Insulin Resistance, Molecular Sequence Data, Obesity, Transcription, Genetic, Tumor Necrosis Factor-alpha, Gene Expression Regulation, Enzymologic, Leptin, Mice, Rats, Protein Tyrosine Phosphatase, Non-Receptor Type 1
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