Chac1 ChaC, cation transport regulator 1 [Mus musculus (house mouse)] - Gene

Summary

Official Symbol: Chac1provided by MGI
Official Full Name: ChaC, cation transport regulator 1provided by MGI
Primary source: MGI:MGI:1916315
See related: Ensembl:ENSMUSG00000027313 AllianceGenome:MGI:1916315
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: 1810008K03Rik
Summary: Enables Notch binding activity. Involved in neurogenesis. Located in trans-Golgi network. Is expressed in embryo. Orthologous to human CHAC1 (ChaC glutathione specific gamma-glutamylcyclotransferase 1). [provided by Alliance of Genome Resources, Apr 2022]
Expression: Broad expression in stomach adult (RPKM 8.7), mammary gland adult (RPKM 8.4) and 23 other tissues See more
Orthologs: human all
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Genomic context

Location:: 2 E5; 2 59.97 cM

Exon count:: 3

Annotation release	Status	Assembly	Chr	Location
RS_2024_02	current	GRCm39 (GCF_000001635.27)	2	NC_000068.8 (119181723..119184807)
108.20200622	previous assembly	GRCm38.p6 (GCF_000001635.26)	2	NC_000068.7 (119351242..119354326)

Chromosome 2 - NC_000068.8 Genomic Context describing neighboring genes

Genomic regions, transcripts, and products

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Genomic Sequence:

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Expression

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See details

Project title: Mouse ENCODE transcriptome data
Description: RNA profiling data sets generated by the Mouse ENCODE project.
BioProject: PRJNA66167
Publication: PMID 25409824
Analysis date: n/a

Bibliography

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GeneRIFs: Gene References Into Functions

What's a GeneRIF?

CHAC1 inactivation is effective to preserve muscle glutathione but is insufficient to protect against muscle wasting in cachexia.
Title: CHAC1 inactivation is effective to preserve muscle glutathione but is insufficient to protect against muscle wasting in cachexia.
CHAC1 exacerbates LPS-induced ferroptosis and apoptosis in HK-2 cells by promoting oxidative stress.
Title: CHAC1 exacerbates LPS-induced ferroptosis and apoptosis in HK-2 cells by promoting oxidative stress.
Study have shown that the 5' UTR of Chac1 plays an important role in expressing the full-length and short form of Chac1, and the expression level of Chac1 protein is predominantly regulated by its ubiquitination.
Title: Translational and post-translational regulation of mouse cation transport regulator homolog 1.
Chac1 expression is detrimental to arsenite-treated cell survival and TRIB3 is critical for restraining the pro-death potential of Chac1 during arsenite stress.
Title: TRIB3 increases cell resistance to arsenite toxicity by limiting the expression of the glutathione-degrading enzyme CHAC1.
Data indicate that Chac1 protein expression was only detected in the presence of MG132, a proteasome inhibitor.
Title: Transcriptional and post-translational regulation of mouse cation transport regulator homolog 1.
The ChaC family is conversed across all phyla and represents a new pathway for glutathione degradation in living cells, and the first cytosolic pathway for glutathione degradation in mammalian cells.
Title: Mammalian proapoptotic factor ChaC1 and its homologues function as γ-glutamyl cyclotransferases acting specifically on glutathione.

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Variation

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Alleles

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

Endonuclease-mediated (4)

General gene information

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Gene Ontology Provided by MGI

Function	Evidence Code	Pubs
enables Notch binding	IDA Inferred from Direct Assay more info	PubMed
enables glutathione specific gamma-glutamylcyclotransferase activity	IBA Inferred from Biological aspect of Ancestor more info
enables glutathione specific gamma-glutamylcyclotransferase activity	ISO Inferred from Sequence Orthology more info
enables lyase activity	IEA Inferred from Electronic Annotation more info

Process	Evidence Code	Pubs
acts_upstream_of_or_within Notch signaling pathway	IEA Inferred from Electronic Annotation more info
acts_upstream_of_or_within apoptotic process	IEA Inferred from Electronic Annotation more info
involved_in glutathione catabolic process	IBA Inferred from Biological aspect of Ancestor more info
involved_in intrinsic apoptotic signaling pathway in response to endoplasmic reticulum stress	ISO Inferred from Sequence Orthology more info
involved_in negative regulation of Notch signaling pathway	ISO Inferred from Sequence Orthology more info
involved_in negative regulation of protein processing	ISO Inferred from Sequence Orthology more info
acts_upstream_of_or_within nervous system development	IEA Inferred from Electronic Annotation more info
involved_in neurogenesis	IMP Inferred from Mutant Phenotype more info	PubMed
acts_upstream_of_or_within response to unfolded protein	IEA Inferred from Electronic Annotation more info

Component	Evidence Code	Pubs
located_in Golgi apparatus	IEA Inferred from Electronic Annotation more info
is_active_in cytoplasm	IBA Inferred from Biological aspect of Ancestor more info
located_in cytosol	ISO Inferred from Sequence Orthology more info
located_in cytosol	TAS Traceable Author Statement more info
located_in trans-Golgi network	IDA Inferred from Direct Assay more info	PubMed

General protein information

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Preferred Names: glutathione-specific gamma-glutamylcyclotransferase 1

Names: ChaC, cation transport regulator-like 1; blocks Notch protein; botch; cation transport regulator-like protein 1; gamma-GCG 1

NP_081205.1

EC 4.3.2.7

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.