The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.
Roles of GRP78 in physiology and cancer
Abstract
As one member of 70 kDa heat shock proteins, glucose‐regulated protein 78 (GRP78) participates in protein folding, transportation and degradation. This sort of capacity can be enhanced by stresses under which GRP78 is induced rapidly. Unlike its homologues, GRP78 presents multifaceted subcellular position: When ER retention, it serves as the switch of unfolded protein response; When mitochondrial binding, it directly interacts with apoptotic executors; When cell surface residing, it recognizes extracellular ligands, transducing proliferative signals, especially in certain tumors. The close correlation between GRP78 and neoplasm provides us further insight into the event of carcinogenesis and cancer cell chemoresistance, indicating its prognostic predicting significance and validating potential therapeutics for clinical usage, especially because its small molecular inhibitors are emerging quickly these years. What's more, GRP78‐related signaling may be helpful for clearer understanding of its biological mechanisms. J. Cell. Biochem. 110: 1299–1305, 2010. © 2010 Wiley‐Liss, Inc.
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Incorporation of a non-human glycan mediates human susceptibility to a bacterial toxin
Byres, E., Paton, A. W., Paton, J. C., Löfling, J. C., Smith, D. F., Wilce, M. C. J., Talbot, U. M., Chong, D. C., Yu, H., Huang, S., et al. (2008) · Nature · doi:10.1038/nature07428 · Cited by 233
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Endoplasmic Reticulum Stress: Its Role in Disease and Novel Prospects for Therapy
Schönthal, A. H. (2012) · Scientifica · doi:10.6064/2012/857516 · Cited by 353
Metadata
- Authors
- Zhang, L., & Zhang, X.
- Venue
- Journal of Cellular Biochemistry
- Publisher
- Wiley
- Published
- 2010-07-14
- Volume
- 110
- Issue
- 6
- Pages
- 1299-1305
- ISSN
- 0730-2312 (ISSN-L)
- 1097-4644
- OpenAlex
- W2089522070
- Cited by
- 184
- References
- 1
- FWCI
- 6.46
- Type
- journal article
- Language
- en
- Open access
- closed
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