Creg1 cellular repressor of E1A-stimulated genes 1 [Mus musculus (house mouse)] - Gene

Summary

Official Symbol: Creg1provided by MGI
Official Full Name: cellular repressor of E1A-stimulated genes 1provided by MGI
Primary source: MGI:MGI:1344382
See related: Ensembl:ENSMUSG00000040713 AllianceGenome:MGI:1344382
Gene type: protein coding
RefSeq status: VALIDATED
Organism: Mus musculus
Lineage: Eukaryota; Metazoa; Chordata; Craniata; Vertebrata; Euteleostomi; Mammalia; Eutheria; Euarchontoglires; Glires; Rodentia; Myomorpha; Muroidea; Muridae; Murinae; Mus; Mus
Also known as: Creg
Summary: Predicted to enable insulin-like growth factor receptor binding activity. Acts upstream of or within several processes, including autophagy; lysosomal lumen acidification; and regulation of DNA-templated transcription. Located in endosome and lysosome. Part of transcription regulator complex. Is expressed in central nervous system; liver; and ureter. Orthologous to human CREG1 (cellular repressor of E1A stimulated genes 1). [provided by Alliance of Genome Resources, Dec 2024]
Expression: Broad expression in placenta adult (RPKM 225.0), liver adult (RPKM 174.7) and 21 other tissues See more
Orthologs: human all
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Genomic context

Location:: 1 H2.3; 1 73.11 cM

Exon count:: 5

Annotation release	Status	Assembly	Chr	Location
RS_2024_02	current	GRCm39 (GCF_000001635.27)	1	NC_000067.7 (165591327..165602878)
108.20200622	previous assembly	GRCm38.p6 (GCF_000001635.26)	1	NC_000067.6 (165763758..165775309)

Chromosome 1 - NC_000067.7 Genomic Context describing neighboring genes

Genomic regions, transcripts, and products

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Genomic Sequence:

Go to nucleotide: Graphics FASTA GenBank

Bibliography

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GeneRIFs: Gene References Into Functions

What's a GeneRIF?

CREG1 deficiency impaired myoblast differentiation and skeletal muscle regeneration.
Title: CREG1 deficiency impaired myoblast differentiation and skeletal muscle regeneration.
The CREG1-FBXO27-LAMP2 axis alleviates diabetic cardiomyopathy by promoting autophagy in cardiomyocytes.
Title: The CREG1-FBXO27-LAMP2 axis alleviates diabetic cardiomyopathy by promoting autophagy in cardiomyocytes.
CREG Protects Retinal Ganglion Cells loss and Retinal Function Impairment Against ischemia-reperfusion Injury in mice via Akt Signaling Pathway.
Title: CREG Protects Retinal Ganglion Cells loss and Retinal Function Impairment Against ischemia-reperfusion Injury in mice via Akt Signaling Pathway.
The role of CREG1 in megakaryocyte maturation and thrombocytopoiesis.
Title: The role of CREG1 in megakaryocyte maturation and thrombocytopoiesis.
CREG1 stimulates AMPK phosphorylation and glucose uptake in skeletal muscle cells.
Title: CREG1 stimulates AMPK phosphorylation and glucose uptake in skeletal muscle cells.
CREG ameliorates the phenotypic switching of cardiac fibroblasts after myocardial infarction via modulation of CDC42.
Title: CREG ameliorates the phenotypic switching of cardiac fibroblasts after myocardial infarction via modulation of CDC42.
Effects of CREG1 on Age-Associated Metabolic Phenotypes and Renal Senescence in Mice.
Title: Effects of CREG1 on Age-Associated Metabolic Phenotypes and Renal Senescence in Mice.
The secreted inhibitor of invasive cell growth CREG1 is negatively regulated by cathepsin proteases.
Title: The secreted inhibitor of invasive cell growth CREG1 is negatively regulated by cathepsin proteases.
findings demonstrate that CREG1 stimulates brown adipocyte formation and browning, ameliorating obesity and its related pathology in vivo.
Title: CREG1 stimulates brown adipocyte formation and ameliorates diet-induced obesity in mice.
effect of CREG1 on Ucp1 promoter activity was also stimulated by retinoic acid. These results strongly suggest that CREG1 plays an important role on the regulation of UCP1 expression and brown adipogenesis
Title: CREG1 promotes uncoupling protein 1 expression and brown adipogenesis in vitro.

Submit: New GeneRIF Correction See all GeneRIFs (23)

Variation

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Alleles

Alleles of this type are documented at Mouse Genome Informatics (MGI)

Endonuclease-mediated (4) 1 citation
Targeted (2) 1 citation

Interactions

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Products	Interactant	Other Gene	Complex	Source	Pubs	Description

General gene information

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Markers

AA755314 (e-PCR)
- UniSTS:158880

AI844869 (e-PCR)
- UniSTS:165119

Gene Ontology Provided by MGI

Function	Evidence Code	Pubs
enables insulin-like growth factor receptor binding	ISO Inferred from Sequence Orthology more info	PubMed
enables transcription factor binding	IDA Inferred from Direct Assay more info	PubMed

Process	Evidence Code	Pubs
acts_upstream_of_or_within autophagy	IMP Inferred from Mutant Phenotype more info	PubMed
acts_upstream_of_or_within endocytosis	IMP Inferred from Mutant Phenotype more info	PubMed
acts_upstream_of_or_within lysosomal lumen acidification	IMP Inferred from Mutant Phenotype more info	PubMed
acts_upstream_of_or_within lysosome organization	IMP Inferred from Mutant Phenotype more info	PubMed
acts_upstream_of_or_within regulation of DNA-templated transcription	IDA Inferred from Direct Assay more info	PubMed

Component	Evidence Code	Pubs
located_in endosome	IDA Inferred from Direct Assay more info	PubMed
is_active_in extracellular space	IBA Inferred from Biological aspect of Ancestor more info
located_in extracellular space	IEA Inferred from Electronic Annotation more info
located_in extracellular space	ISO Inferred from Sequence Orthology more info
located_in lysosome	IDA Inferred from Direct Assay more info	PubMed
part_of transcription regulator complex	IDA Inferred from Direct Assay more info	PubMed

General protein information

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Preferred Names: protein CREG1

NCBI Reference Sequences (RefSeq)

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RefSeqs maintained independently of Annotated Genomes

These reference sequences exist independently of genome builds. Explain

These reference sequences are curated independently of the genome annotation cycle, so their versions may not match the RefSeq versions in the current genome build. Identify version mismatches by comparing the version of the RefSeq in this section to the one reported in Genomic regions, transcripts, and products above.