ArticleThe EMBO journal2001
Hsp72 functions as a natural inhibitory protein of c-Jun N-terminal kinase.
Article in The EMBO journal, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06377358 (Lipolysis of Visceral Reserve Fat Using Tecar Therapy), which is not on this map. Cited by 100 papers.
What it found
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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.
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.
Lipolysis of Visceral Reserve Fat Using Tecar Therapy: Anthropometric, Biochemical and NMR Imaging Study.
Who cites it
100 citing papers in PubMed, 313 citations in OpenAlex.
- Activation of heat shock response to treat obese subjects with type 2 diabetes: a prospective, frequency-escalating, randomized, open-label, triple-arm trial.Scientific reports · 2016Trial
- Exercise reduces cellular stress related to skeletal muscle insulin resistance.Cell stress & chaperones · 2014Trial
- Sage tea drinking improves lipid profile and antioxidant defences in humans.International journal of molecular sciences · 2009Trial
- Heat shock protein 72 (HSP72) modulates glucagon secretion via JNK inhibition in pancreatic α-cells.Diabetology international · 2026Article
- Erythema ab igne-A Potential Cutaneous Marker of Chronic Heat Use in Patients with Endometriosis: A Narrative Literature Review and a Case Report.Life (Basel, Switzerland) · 2025Article
- The role of heat shock protein 70 on oocyte apoptosis during vitrification.Open veterinary journal · 2025Review
- Molecular insights of exercise therapy in disease prevention and treatment.Signal transduction and targeted therapy · 2024Review
- Heat shock response during the resolution of inflammation and its progressive suppression in chronic-degenerative inflammatory diseases.Cell stress & chaperones · 2024Review
- Article
- Nano-chromium picolinate and heat stress enhance insulin sensitivity in cross-bred sheep.Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2023Article
- Bovine sperm HSP-70 molecules: a potential cryo-tolerance marker associated with semen quality and fertility rate.Frontiers in veterinary science · 2023Article
- Exercise training improves obesity-induced inflammatory signaling in rat brown adipose tissue.Biochemistry and biophysics reports · 2022Article
- Heat Shock Proteins (Hsps) in Cellular Homeostasis: A Promising Tool for Health Management in Crustacean Aquaculture.Life (Basel, Switzerland) · 2022Review
- Involvement of heat shock proteins and parkin/α-synuclein axis in Parkinson's disease.Molecular biology reports · 2022Review
- Endothelial HSP72 is not reduced in type 2 diabetes nor is it a key determinant of endothelial insulin sensitivity.American journal of physiology. Regulatory, integrative and comparative physiology · 2022Article
- Overheating or overcooling: heat transfer in the spot to fight against the pandemic obesity.Reviews in endocrine & metabolic disorders · 2021Review
- Molecular Chaperones and miRNAs in Epilepsy: Pathogenic Implications and Therapeutic Prospects.International journal of molecular sciences · 2021Review
- Urocortin 3 overexpression reduces ER stress and heat shock response in 3T3-L1 adipocytes.Scientific reports · 2021Article
- Baicalin alleviates chronic obstructive pulmonary disease through regulation of HSP72-mediated JNK pathway.Molecular medicine (Cambridge, Mass.) · 2021Article
- TheAnnals of translational medicine · 2021Article
40 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hsp72, a major inducible member of the heat shock protein family, can protect cells against many cellular stresses including heat shock. In our present study, we observed that pretreatment of NIH 3T3 cells with mild heat shock (43 degrees C for 20 min) suppressed UV-stimulated c-Jun N-terminal kinase 1 (JNK1) activity. Constitutively overexpressed Hsp72 also inhibited JNK1 activation in NIH 3T3 cells, whereas it did not affect either SEK1 or MEKK1 activity. Both in vitro binding and kinase studies indicated that Hsp72 bound to JNK1 and that the peptide binding domain of Hsp72 was important to the binding and inhibition of JNK1. In vivo binding between endogenous Hsp72 and JNK1 in NIH 3T3 cells was confirmed by co-immunoprecipitation. Hsp72 also inhibited JNK-dependent apoptosis. Hsp72 antisense oligonucleotides blocked Hsp72 production in NIH 3T3 cells in response to mild heat shock and concomitantly abolished the suppressive effect of mild heat shock on UV-induced JNK activation and apoptosis. Collectively, our data suggest strongly that Hsp72 can modulate stress-activated signaling by directly inhibiting JNK.
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Registered trials
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.