C1qa complement component 1, q subcomponent, alpha polypeptide [Mus musculus (house mouse)] - Gene

Summary

Official Symbol: C1qaprovided by MGI
Official Full Name: complement component 1, q subcomponent, alpha polypeptideprovided by MGI
Primary source: MGI:MGI:88223
See related: Ensembl:ENSMUSG00000036887 AllianceGenome:MGI:88223
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: C1q; Adic
Summary: Involved in complement-mediated synapse pruning; glial cell activation; and nervous system development. Acts upstream of or within complement activation, classical pathway. Located in postsynapse. Is active in glutamatergic synapse. Is extrinsic component of postsynaptic membrane and extrinsic component of presynaptic membrane. Is expressed in several structures, including brain; genitourinary system; lung; pancreas; and vestibular component mesenchyme. Used to study epilepsy and systemic lupus erythematosus. Human ortholog(s) of this gene implicated in glomerulonephritis. Orthologous to human C1QA (complement C1q A chain). [provided by Alliance of Genome Resources, Nov 2024]
Expression: Ubiquitous expression in mammary gland adult (RPKM 87.8), spleen adult (RPKM 86.7) and 25 other tissues See more
Orthologs: human all
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Genomic context

Location:: 4 D3; 4 69.05 cM

Exon count:: 3

Annotation release	Status	Assembly	Chr	Location
RS_2024_02	current	GRCm39 (GCF_000001635.27)	4	NC_000070.7 (136623227..136626155, complement)
108.20200622	previous assembly	GRCm38.p6 (GCF_000001635.26)	4	NC_000070.6 (136895916..136898844, complement)

Chromosome 4 - NC_000070.7 Genomic Context describing neighboring genes

Genomic regions, transcripts, and products

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Go to reference sequence details

Genomic Sequence:

Go to nucleotide: Graphics FASTA GenBank

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?

Complement Factor C1q Mediates Vascular Endothelial Dysfunction in STZ-Induced Diabetic Mice.
Title: Complement Factor C1q Mediates Vascular Endothelial Dysfunction in STZ-Induced Diabetic Mice.
C1q/Tumor Necrosis Factor-Related Protein-9 Is a Novel Vasculoprotective Cytokine That Restores High Glucose-Suppressed Endothelial Progenitor Cell Functions by Activating the Endothelial Nitric Oxide Synthase.
Title: C1q/Tumor Necrosis Factor-Related Protein-9 Is a Novel Vasculoprotective Cytokine That Restores High Glucose-Suppressed Endothelial Progenitor Cell Functions by Activating the Endothelial Nitric Oxide Synthase.
Cognitive impairment in Alzheimer's disease FAD[4T] mouse model: Synaptic loss facilitated by activated microglia via C1qA.
Title: Cognitive impairment in Alzheimer's disease FAD(4T) mouse model: Synaptic loss facilitated by activated microglia via C1qA.
Complement C1q essential for aeroallergen sensitization via CSF1R[+] conventional dendritic cells type 2.
Title: Complement C1q essential for aeroallergen sensitization via CSF1R(+) conventional dendritic cells type 2.
Influence of complement protein C1q or complement receptor C5aR1 on gut microbiota composition in wildtype and Alzheimer's mouse models.
Title: Influence of complement protein C1q or complement receptor C5aR1 on gut microbiota composition in wildtype and Alzheimer's mouse models.
Complement C1q drives microglia-dependent synaptic loss and cognitive impairments in a mouse model of lipopolysaccharide-induced neuroinflammation.
Title: Complement C1q drives microglia-dependent synaptic loss and cognitive impairments in a mouse model of lipopolysaccharide-induced neuroinflammation.
A tick C1q protein alters infectivity of the Lyme disease agent by modulating interferon gamma.
Title: A tick C1q protein alters infectivity of the Lyme disease agent by modulating interferon γ.
Fecal microbiota transplantation ameliorates atherosclerosis in mice with C1q/TNF-related protein 9 genetic deficiency.
Title: Fecal microbiota transplantation ameliorates atherosclerosis in mice with C1q/TNF-related protein 9 genetic deficiency.
C1q and SRPX2 regulate microglia mediated synapse elimination during early development in the visual thalamus but not the visual cortex.
Title: C1q and SRPX2 regulate microglia mediated synapse elimination during early development in the visual thalamus but not the visual cortex.
C1q inhibits differentiation of oligodendrocyte progenitor cells via Wnt/beta-catenin signaling activation in a cuprizone-induced mouse model of multiple sclerosis.
Title: C1q inhibits differentiation of oligodendrocyte progenitor cells via Wnt/β-catenin signaling activation in a cuprizone-induced mouse model of multiple sclerosis.

Submit: New GeneRIF Correction See all GeneRIFs (71)

Variation

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Alleles

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

Endonuclease-mediated (7)
Targeted (6) 1 citation

Interactions

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Products	Interactant	Other Gene	Complex	Source	Pubs	Description

General gene information

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Markers

X58861 (e-PCR)
- UniSTS:159309

NoName (e-PCR)
- UniSTS:485504

AI255395 (e-PCR)
- UniSTS:179092

Gene Ontology Provided by MGI

Function	Evidence Code	Pubs
enables protein binding	IPI Inferred from Physical Interaction more info	PubMed

Process	Evidence Code	Pubs
involved_in astrocyte activation	IGI Inferred from Genetic Interaction more info	PubMed
acts_upstream_of_or_within complement activation, classical pathway	IMP Inferred from Mutant Phenotype more info	PubMed
involved_in complement activation, classical pathway	ISO Inferred from Sequence Orthology more info
involved_in complement activation, classical pathway	NAS Non-traceable Author Statement more info	PubMed
involved_in complement-mediated synapse pruning	IMP Inferred from Mutant Phenotype more info	PubMed
involved_in innate immune response	IEA Inferred from Electronic Annotation more info
involved_in microglial cell activation	IGI Inferred from Genetic Interaction more info	PubMed
involved_in neuron remodeling	IMP Inferred from Mutant Phenotype more info	PubMed
involved_in synapse organization	IGI Inferred from Genetic Interaction more info	PubMed
involved_in synapse pruning	IGI Inferred from Genetic Interaction more info	PubMed
involved_in vertebrate eye-specific patterning	IMP Inferred from Mutant Phenotype more info	PubMed

Component	Evidence Code	Pubs
part_of collagen trimer	IEA Inferred from Electronic Annotation more info
part_of complement component C1 complex	NAS Non-traceable Author Statement more info	PubMed
part_of complement component C1q complex	ISO Inferred from Sequence Orthology more info
located_in extracellular region	ISO Inferred from Sequence Orthology more info
located_in extracellular region	NAS Non-traceable Author Statement more info	PubMed
located_in extracellular space	HDA more info	PubMed
is_active_in extrinsic component of postsynaptic membrane	IDA Inferred from Direct Assay more info	PubMed
is_active_in extrinsic component of presynaptic membrane	IDA Inferred from Direct Assay more info	PubMed
is_active_in glutamatergic synapse	IDA Inferred from Direct Assay more info	PubMed
located_in postsynapse	IGI Inferred from Genetic Interaction more info	PubMed
located_in synapse	IDA Inferred from Direct Assay more info	PubMed
located_in synapse	IGI Inferred from Genetic Interaction more info	PubMed
located_in synapse	ISO Inferred from Sequence Orthology more info

General protein information

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Preferred Names: complement C1q subcomponent subunit A

Names: adiponectin c

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.