Sel1l negatively regulates Pre-Notch exit from endoplasmic reticulum

Stable Identifier
R-MMU-2032750
Type
Reaction [transition]
Species
Mus musculus
Compartment
General
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Sel1l negatively regulates Pre-Notch exit from endoplasmic reticulum

Sel1l encodes an endoplasmic reticulum membrane protein that is part of the ERAD (endoplasmic reticulum associated degradation) system, which performs quality control and triggers degradation of misfolded proteins (Francisco et al. 2010). Sel1l is a homolog of C. elegans sel-1, identified as a negative regulator of C. elegans Notch homolog lin-12 (Sundaram et al. 1993). Homozygous Sel1l mutant mouse embryos exhibit defects in differentiation of pancreatic cells and pancreas development that are rescued by pharmacological inhibition of Notch signaling (Li et al. 2010).

Literature References
PubMed ID Title Journal Year
20197277 Deficiency of suppressor enhancer Lin12 1 like (SEL1L) in mice leads to systemic endoplasmic reticulum stress and embryonic lethality

Francisco, AB, Singh, R, Li, S, Vani, AK, Yang, L, Munroe, RJ, Diaferia, G, Cardano, M, Biunno, I, Qi, L, Schimenti, JC, Long, Q

J Biol Chem 2010
20170518 SEL1L deficiency impairs growth and differentiation of pancreatic epithelial cells

Li, S, Francisco, AB, Munroe, RJ, Schimenti, JC, Long, Q

BMC Dev Biol 2010
8293978 Suppressors of a lin-12 hypomorph define genes that interact with both lin-12 and glp-1 in Caenorhabditis elegans

Sundaram, M, Greenwald, I

Genetics 1993
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