The DOI matches its Crossref record; 20 of the 20 references it cites were found in a registry or an index.
CHOP is a multifunctional transcription factor in the ER stress response
Abstract
The accumulation of unfolded proteins in the endoplasmic reticulum (ER) induces ER stress. To restore ER homeostasis, cells possess a highly specific ER quality-control system called the unfold protein response (UPR). In the case of prolonged ER stress or UPR malfunction, apoptosis signalling is activated. This ER stress-induced apoptosis has been implicated in the pathogenesis of several conformational diseases. CCAAT-enhancer-binding protein homologous protein (CHOP) is induced by ER stress and mediates apoptosis. Recent studies by the Gotoh group have shown that the CHOP pathway is also involved in ER stress-induced cytokine production in macrophages. The multifunctional roles of CHOP in the ER stress response are discussed below.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Dynamic interaction of BiP and ER stress transducers in the unfolded-protein response
Bertolotti, A., Zhang, Y., Hendershot, L. M., Harding, H. P., & Ron, D. (2000) · Nature Cell Biology · doi:10.1038/35014014 · Cited by 2,860
Roles of CHOP/GADD153 in endoplasmic reticulum stress
Oyadomari, S., & Mori, M. (2004) · Cell Death & Differentiation · doi:10.1038/sj.cdd.4401373 · Cited by 2,828
Integrating the mechanisms of apoptosis induced by endoplasmic reticulum stress
Tabas, I., & Ron, D. (2011) · Nature Cell Biology · doi:10.1038/ncb0311-184 · Cited by 2,598
Non-canonical inflammasome activation targets caspase-11
Kayagaki, N., Warming, S., Lamkanfi, M., Walle, L. V., Louie, S., Dong, J., Newton, K., Qu, Y., Liu, J., Heldens, S., et al. (2011) · Nature · doi:10.1038/nature10558 · Cited by 2,530
Harding, H. P., Zhang, Y., Bertolotti, A., Zeng, H., & Ron, D. (2000) · Molecular Cell · doi:10.1016/s1097-2765(00)80330-5 · Cited by 2,021
Cell death and endoplasmic reticulum stress: disease relevance and therapeutic opportunities
Kim, I., Xu, W., & Reed, J. C. (2008) · Nature Reviews Drug Discovery · doi:10.1038/nrd2755 · Cited by 1,817
Endoplasmic Reticulum Stress Signaling in Disease
Marciniak, S. J., & Ron, D. (2006) · Physiological Reviews · doi:10.1152/physrev.00015.2006 · Cited by 945
Yamaguchi, H., & Wang, H.-G. (2004) · Journal of Biological Chemistry · doi:10.1074/jbc.m406933200 · Cited by 831
Li, G., Mongillo, M., Chin, K.-T., Harding, H., Ron, D., Marks, A. R., & Tabas, I. (2009) · Journal of Cell Biology · doi:10.1083/jcb.200904060 · Cited by 595
Cytoprotection by pre‐emptive conditional phosphorylation of translation initiation factor 2
Lu, P. D., Jousse, C., Marciniak, S. J., Zhang, Y., Novoa, I., Scheuner, D., Kaufman, R. J., Ron, D., & Harding, H. P. (2004) · The EMBO Journal · doi:10.1038/sj.emboj.7600030 · Cited by 382
Cited by
Decoding cell death signals in liver inflammation
Brenner, C., Galluzzi, L., Kepp, O., & Kroemer, G. (2013) · Journal of Hepatology · doi:10.1016/j.jhep.2013.03.033 · Cited by 1,022
Shi, C.-S., Nabar, N. R., Huang, N.-N., & Kehrl, J. H. (2019) · Cell Death Discovery · doi:10.1038/s41420-019-0181-7 · Cited by 404
McSweeney, K. R., Gadanec, L. K., Qaradakhi, T., Ali, B. A., Zulli, A., & Apostolopoulos, V. (2021) · Cancers · doi:10.3390/cancers13071572 · Cited by 363
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
Piao, M. J., Ahn, M. J., Kang, K. A., Ryu, Y. S., Hyun, Y. J., Shilnikova, K., Zhen, A. X., Jeong, J. W., Choi, Y. H., Kang, H. K., et al. (2018) · Archives of Toxicology · doi:10.1007/s00204-018-2197-9 · Cited by 339
“ER stress promotes the expression of C/EBP homologous protein (CHOP), which mediates apoptosis (Nishitoh 2012), and of the ER chaperone and signaling regulator GRP78, which activates protein kinase R-like ER kinase (PERK) through phosphorylation.”
Metadata
- Authors
- Nishitoh, H.
- Venue
- Journal of Biochemistry
- Publisher
- Oxford University Press (OUP)
- Published
- 2011-12-30
- Volume
- 151
- Issue
- 3
- Pages
- 217-219
- ISSN
- 0021-924X (ISSN-L)
- OpenAlex
- W2113254662
- Cited by
- 469
- References
- 20
- FWCI
- 3.54
- Type
- journal article
- Language
- en
- Open access
- closed
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: CHOP is a multifunctional transcription factor in the ER stress response. https://app.cochat.ai/papers/10.1093/jb/mvr143
- The paper
- Nishitoh, H. (2012). CHOP is a multifunctional transcription factor in the ER stress response. Journal of Biochemistry. https://doi.org/10.1093/jb/mvr143
Data sources
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.