Rprm reprimo, TP53 dependent G2 arrest mediator candidate [Mus musculus (house mouse)] - Gene

Summary

Official Symbol: Rprmprovided by MGI
Official Full Name: reprimo, TP53 dependent G2 arrest mediator candidateprovided by MGI
Primary source: MGI:MGI:1915124
See related: Ensembl:ENSMUSG00000075334 AllianceGenome:MGI:1915124
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: Reprimo; 2410012A13Rik
Summary: Acts upstream of or within regulation of mitotic cell cycle. Located in cytoplasm. Is expressed in several structures, including autopod; central nervous system; glans of male genital tubercle; metanephros; and sensory organ. Orthologous to human RPRM (reprimo, TP53 dependent G2 arrest mediator homolog). [provided by Alliance of Genome Resources, Apr 2022]
Orthologs: human all
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Genomic context

Location:: 2 C1.1; 2 30.69 cM

Exon count:: 1

Annotation release	Status	Assembly	Chr	Location
RS_2024_02	current	GRCm39 (GCF_000001635.27)	2	NC_000068.8 (53974105..53975564, complement)
108.20200622	previous assembly	GRCm38.p6 (GCF_000001635.26)	2	NC_000068.7 (54084093..54085552, complement)

Chromosome 2 - NC_000068.8 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?

Reprimo (RPRM) mediates neuronal ferroptosis via CREB-Nrf2/SCD1 pathways in radiation-induced brain injury.
Title: Reprimo (RPRM) mediates neuronal ferroptosis via CREB-Nrf2/SCD1 pathways in radiation-induced brain injury.
RPRM deletion preserves hematopoietic regeneration by promoting EGFR-dependent DNA repair and hematopoietic stem cell proliferation post ionizing radiation.
Title: RPRM deletion preserves hematopoietic regeneration by promoting EGFR-dependent DNA repair and hematopoietic stem cell proliferation post ionizing radiation.
RPRM is transiently up-regulated at a posttranscriptional level in times of cellular stress to restrict cell survival, proliferation, and tumor formation
Title: Reprimo (RPRM) is a novel tumor suppressor in pituitary tumors and regulates survival, proliferation, and tumorigenicity.
Mice deficient in p53 show less degeneration of spermatogenesis was observed in p53-null-jsd mice than jsd single mutants.
Title: p53-dependent apoptosis in the inhibition of spermatogonial differentiation in juvenile spermatogonial depletion (Utp14bjsd) mice.
tp53 activation occurs at a posttranslational level via chloroquine-dependent phosphorylation of the checkpoint protein {ATM)leading to ATM-dependent phosphorylation of tp53 kinase, and mediating resistance to mammary carcinogenesis.
Title: Ataxia telangiectasia-mutated and p53 are potential mediators of chloroquine-induced resistance to mammary carcinogenesis.
targeting p53 to mitochondria does confer a significant growth disadvantage in B-lymphomas expressing various point mutants of p53, resulting in efficient apoptosis induction in vitro and in vivo in mice
Title: Mitochondrially targeted wild-type p53 suppresses growth of mutant p53 lymphomas in vivo.
p53(R273H) binds directly to the relaxin promoter, further confirming a role for H2 relaxin signaling in p53(R273H)-mediated androgen-independent prostate cancer
Title: The R273H p53 mutation can facilitate the androgen-independent growth of LNCaP by a mechanism that involves H2 relaxin and its cognate receptor LGR7.
Induction by DNA damage and hypoxia suggest IGFBP-3 plays a role in the physiologic protection against aberrant cell growth.
Title: p53-Dependent and p53-independent induction of insulin-like growth factor binding protein-3 by deoxyribonucleic acid damage and hypoxia.
Oral administration of green tea or topical caffeine immediately after discontinuation of UVB treatment enhanced the rate and extent of disappearance of the mutant p53-positive patches on skin of hairless mice.
Title: Administration of green tea or caffeine enhances the disappearance of UVB-induced patches of mutant p53 positive epidermal cells in SKH-1 mice.
In p53-null cells, this peptide derepresses p73, causing p73-mediated gene activation and death. Moreover, delivery of a transgene expressing this peptide caused tumors.
Title: A p53-derived apoptotic peptide derepresses p73 to cause tumor regression in vivo.

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Variation

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Alleles

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

Endonuclease-mediated (1)

General gene information

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Gene Ontology Provided by MGI

Function	Evidence Code	Pubs
enables molecular_function	ND No biological Data available more info

Process	Evidence Code	Pubs
acts_upstream_of_or_within regulation of cell cycle	IDA Inferred from Direct Assay more info	PubMed
involved_in regulation of mitotic cell cycle	IBA Inferred from Biological aspect of Ancestor more info
acts_upstream_of_or_within regulation of mitotic cell cycle	IDA Inferred from Direct Assay more info	PubMed

Component	Evidence Code	Pubs
is_active_in cytoplasm	IBA Inferred from Biological aspect of Ancestor more info
located_in cytoplasm	IDA Inferred from Direct Assay more info	PubMed
located_in membrane	IEA Inferred from Electronic Annotation more info

General protein information

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Preferred Names: protein reprimo

Names: reprimo, TP53 dependant G2 arrest mediator candidate

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.