Endoplasmic reticulum stress disrupts signaling via altered processing of transmembrane receptors
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985904%3A_____%2F25%3A00637010" target="_blank" >RIV/67985904:_____/25:00637010 - isvavai.cz</a>
Alternative codes found
RIV/68081707:_____/25:00637010 RIV/00216224:14110/25:00141289 RIV/65269705:_____/25:00081969
Result on the web
<a href="https://biosignaling.biomedcentral.com/articles/10.1186/s12964-025-02208-w" target="_blank" >https://biosignaling.biomedcentral.com/articles/10.1186/s12964-025-02208-w</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1186/s12964-025-02208-w" target="_blank" >10.1186/s12964-025-02208-w</a>
Alternative languages
Result language
angličtina
Original language name
Endoplasmic reticulum stress disrupts signaling via altered processing of transmembrane receptors
Original language description
Cell communication systems based on polypeptide ligands use transmembrane receptors to transmit signals across the plasma membrane. In their biogenesis, receptors depend on the endoplasmic reticulum (ER)-Golgi system for folding, maturation, transport and localization to the cell surface. ER stress, caused by protein overproduction and misfolding, is a well-known pathology in neurodegeneration, cancer and numerous other diseases. How ER stress affects cell communication via transmembrane receptors is largely unknown. In disease models of multiple myeloma, chronic lymphocytic leukemia and osteogenesis imperfecta, we show that ER stress leads to loss of the mature transmembrane receptors FGFR3, ROR1, FGFR1, LRP6, FZD5 and PTH1R at the cell surface, resulting in impaired downstream signaling. This is caused by downregulation of receptor production and increased intracellular retention of immature receptor forms. Reduction of ER stress by treatment of cells with the chemical chaperone tauroursodeoxycholic acid or by expression of the chaperone protein BiP resulted in restoration of receptor maturation and signaling. We show a previously unappreciated pathological effect of ER stress, impaired cellular communication due to altered receptor processing. Our findings have implications for disease mechanisms related to ER stress and are particularly important when receptor-based pharmacological approaches are used for treatment.
Czech name
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Czech description
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Classification
Type
J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database
CEP classification
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OECD FORD branch
10601 - Cell biology
Result continuities
Project
Result was created during the realization of more than one project. More information in the Projects tab.
Continuities
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Others
Publication year
2025
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Cell communication and signaling : CCS
ISSN
1478-811X
e-ISSN
1478-811X
Volume of the periodical
23
Issue of the periodical within the volume
1
Country of publishing house
GB - UNITED KINGDOM
Number of pages
17
Pages from-to
209
UT code for WoS article
001479437500002
EID of the result in the Scopus database
2-s2.0-105003875911