ArticleCell stress & chaperones2003
Induction of heat shock protein gp96 by immune cytokines.
Article in Cell stress & chaperones, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- What is the role of heat shock protein in abdominal organ transplantation?Einstein (Sao Paulo, Brazil) · 2022Article
- GRP94 Is Involved in the Lipid Phenotype of Brain Metastatic Cells.International journal of molecular sciences · 2019Article
- Endoplasmic reticulum stress signalling - from basic mechanisms to clinical applications.The FEBS journal · 2019Review
- Gp96 Peptide Antagonist gp96-II Confers Therapeutic Effects in Murine Intestinal Inflammation.Frontiers in immunology · 2017Article
- Clients and Oncogenic Roles of Molecular Chaperone gp96/grp94.Current topics in medicinal chemistry · 2016Review
- Fas signaling in macrophages promotes chronicity in K/BxN serum-induced arthritis.Arthritis & rheumatology (Hoboken, N.J.) · 2014Article
- Do reciprocal interactions between cell stress proteins and cytokines create a new intra-/extra-cellular signalling nexus?Cell stress & chaperones · 2013Article
- Article
- Heat shock protein 96 is elevated in rheumatoid arthritis and activates macrophages primarily via TLR2 signaling.Journal of immunology (Baltimore, Md. : 1950) · 2009Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cytokines play a major role in regulating both humoral and cell-mediated immune responses. Recent advances in our understanding of cell-mediated immune responses have focused on the antigen presentation machinery and the proteins in the endoplasmic reticulum (ER). These proteins help the formation and stabilization of the major histocompatibility complex (MHC)-peptide interaction. A 96-kDa, ER-resident glycoprotein (gp96) is being evaluated as a therapeutic agent in cancer because of its ability to associate with a vast number of cellular peptides irrespective of size or sequence. Because the antigen presentation complex is assembled in the ER and a number of ER-resident proteins are modulated by cytokines, it is important to examine the regulation of gp96 in response to immune cytokines interferon gamma (IFN-gamma), and interleukin 2 (IL-2). Defects in signaling pathway in either of the cytokines can result in suboptimal immune response. We examined the effect of the cytokines IFN-gamma and IL-2 on the induction of gp96 in different cancer cell lines and examined the induction of DNA-binding proteins that recognize gamma interferon-activating sequence (GAS), present in the promoter region of gp96. The induction of GAS binding protein correlated with the induction of STAT 1 protein, a transcriptional regulator and mediator of IFN-gamma-mediated gene expression. The use of cytokines in inducing gp96 levels may have significance in maintaining high levels of gp96 for a sustained immune response.
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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.