Faim Fas apoptotic inhibitory molecule [Rattus norvegicus (Norway rat)] - Gene

Summary

Official Symbol: Faimprovided by RGD
Official Full Name: Fas apoptotic inhibitory moleculeprovided by RGD
Primary source: RGD:620572
See related: EnsemblRapid:ENSRNOG00000030069 AllianceGenome:RGD:620572
Gene type: protein coding
RefSeq status: PROVISIONAL
Organism: Rattus norvegicus
Lineage: Eukaryota; Metazoa; Chordata; Craniata; Vertebrata; Euteleostomi; Mammalia; Eutheria; Euarchontoglires; Glires; Rodentia; Myomorpha; Muroidea; Muridae; Murinae; Rattus
Summary: Involved in positive regulation of canonical NF-kappaB signal transduction and positive regulation of neurogenesis. Predicted to be located in cytoplasm. Orthologous to human FAIM (Fas apoptotic inhibitory molecule). [provided by Alliance of Genome Resources, Jan 2025]
Expression: Biased expression in Heart (RPKM 39.5), Kidney (RPKM 38.1) and 9 other tissues See more
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Genomic context

Location:: 8q31

Exon count:: 8

Annotation release	Status	Assembly	Chr	Location
RS_2024_02	current	GRCr8 (GCF_036323735.1)	8	NC_086026.1 (108423259..108445365)
RS_2023_06	previous assembly	mRatBN7.2 (GCF_015227675.2)	8	NC_051343.1 (99543877..99569499)
106	previous assembly	Rnor_6.0 (GCF_000001895.5)	8	NC_005107.4 (107225119..107247228)

Chromosome 8 - NC_086026.1 Genomic Context describing neighboring genes

Genomic regions, transcripts, and products

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Genomic Sequence:

Go to nucleotide: Graphics FASTA GenBank

Expression

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See details

Project title: A rat RNA-Seq transcriptomic BodyMap across 11 organs and 4 developmental stages
Description: 320 RNA samples isolated from 11 organs (adrenal gland, brain, heart, kidney, liver, lung, muscle, spleen, thymus, and testes or uterus) from both sexes of Fischer 344 rats across four developmental stages (2-, 6-, 21-, and 104-weeks-old)
BioProject: PRJNA238328
Publication: PMID 24510058
Analysis date: Mon Jun 6 17:44:12 2016

Bibliography

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GeneRIFs: Gene References Into Functions

What's a GeneRIF?

the anti-apoptotic effect of SRT1720 was mitigated by FAIM knockdown with a small interfering RNA-targeted FAIM. These results indicated that pretreatment with SRT1720 improves survival of aged hMSCs, and enhances their therapeutic efficacy for rat myocardial infarction (MI).
Title: SRT1720 promotes survival of aged human mesenchymal stem cells via FAIM: a pharmacological strategy to improve stem cell-based therapy for rat myocardial infarction.
Whereas FAIM overexpression greatly enhanced neurite outgrowth from PC12 cells and sympathetic neurons grown with nerve growth factor, reduction of endogenous FAIM levels by RNAi decreased neurite outgrowth in these cells
Title: The death receptor antagonist FAIM promotes neurite outgrowth by a mechanism that depends on ERK and NF-kapp B signaling.

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Interactions

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Products	Interactant	Other Gene	Complex	Source	Pubs	Description

General gene information

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Markers

RH132415 (e-PCR)
- UniSTS:215698

Faim (e-PCR), detects polymorphism
- UniSTS:256468

BE112969 (e-PCR)
- UniSTS:246250

Gene Ontology Provided by RGD

Process	Evidence Code	Pubs
involved_in apoptotic process	IEA Inferred from Electronic Annotation more info
involved_in negative regulation of extrinsic apoptotic signaling pathway via death domain receptors	IBA Inferred from Biological aspect of Ancestor more info
acts_upstream_of_or_within negative regulation of extrinsic apoptotic signaling pathway via death domain receptors	ISO Inferred from Sequence Orthology more info
involved_in positive regulation of canonical NF-kappaB signal transduction	IMP Inferred from Mutant Phenotype more info	PubMed
involved_in positive regulation of neurogenesis	IMP Inferred from Mutant Phenotype more info	PubMed

Component	Evidence Code	Pubs
located_in cytoplasm	IEA Inferred from Electronic Annotation more info

General protein information

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Preferred Names: fas apoptotic inhibitory molecule 1

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.