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Cellular repressor of E1A-stimulated genes 1 (CREG1)
- Target
- CREG1
- Molecular classification
- Other (glycoprotein, non-enzymatic, structurally similar to oxidoreductases but lacking enzymatic activity)
01
Overview
Cellular repressor of E1A-stimulated genes 1 (CREG1) is a secreted, predominantly intracellular 220 amino acid glycoprotein that is structurally similar to oxidoreductases but lacks enzymatic activity due to an inability to bind flavin mononucleotide. CREG1 functions as an antagonist to the adenovirus E1A protein and Ras-mediated cellular transformation, acting as a repressor of cell proliferation and an inducer of cellular differentiation. CREG1 localizes mainly to the endocytic-lysosomal compartment, where it undergoes post-translational modifications and interacts with the mannose-6-phosphate/insulin-like growth factor-2 receptor (M6P/IGF2R) and exocyst Sec8. Its expression is tightly regulated during development, and it plays an essential role in embryogenesis, as knockout models are lethal in early development. Beyond development, CREG1 influences metabolism, with reduced levels causing susceptibility to diet-induced obesity and insulin resistance. Although it is not a therapeutic target at this time, CREG1 is biologically notable for its role in cell growth regulation, tissue homeostasis, and possibly cancer suppression.
- Other names
- CREGProtein CREG1UNQ727/PRO1409Cellular repressor of E1A-stimulated genes 1
02
Biological functions
Inhibition of cell proliferationInduction of cell differentiation and senescenceEssential for normal embryonic development (developmental regulation)Possible role in regulation of transcription mediated by E2F and pRb interaction
03
Disease associations
Developmental disorders (embryonic lethality in knockout models)Metabolic disease (promotes susceptibility to obesity, steatosis, insulin resistance in liver-specific knockouts)Cancer (regulates transformation and proliferation; overexpression inhibits transformation by E1A and Ras)Other (possible role in tissue homeostasis)
04
Safety considerations
Essential for embryonic development; global knockout causes early embryonic lethality in miceLoss of function may contribute to metabolic dysfunction (e.g., hepatic steatosis, insulin resistance)
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