The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
ER chaperones in mammalian development and human diseases
Open accessAbstract
The field of endoplasmic reticulum (ER) stress in mammalian cells has expanded rapidly during the past decade, contributing to understanding of the molecular pathways that allow cells to adapt to perturbations in ER homeostasis. One major mechanism is mediated by molecular ER chaperones which are critical not only for quality control of proteins processed in the ER, but also for regulation of ER signaling in response to ER stress. Here, we summarized the properties and functions of GRP78/BiP, GRP94/gp96, GRP170/ORP150, GRP58/ERp57, PDI, ERp72, calnexin, calreticulin, EDEM, Herp and co‐chaperones SIL1 and P58 IPK and their role in development and diseases. Many of the new insights are derived from recently constructed mouse models where the genes encoding the chaperones are genetically altered, providing invaluable tools for examining the physiological involvement of the ER chaperones in vivo.
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Cites
Atherosclerosis--an inflammatory disease
Ross, R. (1999) · New England Journal of Medicine · doi:10.1056/nejm199901143400207 · Cited by 21,725
ER stress and neurodegenerative diseases
Lindholm, D., Wootz, H., & Korhonen, L. (2006) · Cell Death & Differentiation · doi:10.1038/sj.cdd.4401778 · Cited by 882
Yan, W., Frank, C. L., Korth, M. J., Sopher, B. L., Novoa, I., Ron, D., & Katze, M. G. (2002) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.252341799 · Cited by 385
Fernandez, P. M., Tabbara, S. O., Jacobs, L. K., Manning, F. C. R., Tsangaris, T. N., Schwartz, A. M., Kennedy, K. A., & Patierno, S. R. (2000) · Breast Cancer Research and Treatment · doi:10.1023/a:1006332011207 · Cited by 338
ER Stress, Hypoxia Tolerance and Tumor Progression
Koumenis, C. (2006) · Current Molecular Medicine · doi:10.2174/156652406775574604 · Cited by 231 · cited 1×
“Due to hypoxic conditions and glucose deprivation caused by poor vascularization, the microenvironment of tumors represents physiological ER stress and the UPR is activated for the survival of tumor cells [67,68].”
BackgroundContrasting functions of calreticulin and calnexin in glycoprotein folding and ER quality control
Molinari, M., Eriksson, K. K., Calanca, V., Galli, C., Cresswell, P., Michalak, M., & Helenius, A. (2004) · Molecular Cell · doi:10.1016/s1097-2765(03)00494-5 · Cited by 221
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Cited by
Cellular Stress Responses: Cell Survival and Cell Death
Fulda, S., Gorman, A. M., Hori, O., & Samali, A. (2010) · International Journal of Cell Biology · doi:10.1155/2010/214074 · Cited by 1,519
The Role for Endoplasmic Reticulum Stress in Diabetes Mellitus
Eizirik, D. L., Cardozo, A. K., & Cnop, M. (2008) · Endocrine Reviews · doi:10.1210/er.2007-0015 · Cited by 1,173
Biological and Chemical Approaches to Diseases of Proteostasis Deficiency
Powers, E. T., Morimoto, R. I., Dillin, A., Kelly, J. W., & Balch, W. E. (2009) · Annual Review of Biochemistry · doi:10.1146/annurev.biochem.052308.114844 · Cited by 1,149
NRF2 and KEAP1 mutations: permanent activation of an adaptive response in cancer
Hayes, J. D., & McMahon, M. (2009) · Trends in Biochemical Sciences · doi:10.1016/j.tibs.2008.12.008 · Cited by 869
Glucose-regulated proteins in cancer: molecular mechanisms and therapeutic potential
Lee, A. S. (2014) · Nature Reviews Cancer · doi:10.1038/nrc3701 · Cited by 587
Self-citation
Metadata
- Authors
- Ni, M., & Lee, A. S.
- Venue
- FEBS Letters
- Publisher
- Wiley
- Published
- 2007-04-25
- Volume
- 581
- Issue
- 19
- Pages
- 3641-3651
- ISSN
- 0014-5793 (ISSN-L)
- 1873-3468
- OpenAlex
- W2139396663
- Cited by
- 735
- References
- 7
- FWCI
- 21.94
- Type
- journal article
- Language
- en
- Open access
- bronze
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
