Cfp complement factor properdin [Mus musculus (house mouse)] - Gene

Summary

Official Symbol: Cfpprovided by MGI
Official Full Name: complement factor properdinprovided by MGI
Primary source: MGI:MGI:97545
See related: Ensembl:ENSMUSG00000001128 AllianceGenome:MGI:97545
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: Pfc; BCFG
Summary: Involved in complement activation, alternative pathway. Located in extracellular space and secretory granule. Is expressed in embryo; liver left lobe; and liver right lobe. Human ortholog(s) of this gene implicated in X-linked properdin deficiency. Orthologous to human CFP (complement factor properdin). [provided by Alliance of Genome Resources, Dec 2024]
Expression: Broad expression in spleen adult (RPKM 86.6), mammary gland adult (RPKM 42.7) and 25 other tissues See more
Orthologs: human all
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Genomic context

Location:: X A1.3; X 16.44 cM

Exon count:: 9

Annotation release	Status	Assembly	Chr	Location
RS_2024_02	current	GRCm39 (GCF_000001635.27)	X	NC_000086.8 (20791693..20797794, complement)
108.20200622	previous assembly	GRCm38.p6 (GCF_000001635.26)	X	NC_000086.7 (20925454..20931555, complement)

Chromosome X - NC_000086.8 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?

Infiltrating myeloid cell-derived properdin markedly promotes microglia-mediated neuroinflammation after ischemic stroke.
Title: Infiltrating myeloid cell-derived properdin markedly promotes microglia-mediated neuroinflammation after ischemic stroke.
HBSP improves kidney ischemia-reperfusion injury and promotes repair in properdin deficient mice via enhancing phagocytosis of tubular epithelial cells.
Title: HBSP improves kidney ischemia-reperfusion injury and promotes repair in properdin deficient mice via enhancing phagocytosis of tubular epithelial cells.
Properdin Deficiency Impairs Phagocytosis and Enhances Injury at Kidney Repair Phase Post Ischemia-Reperfusion.
Title: Properdin Deficiency Impairs Phagocytosis and Enhances Injury at Kidney Repair Phase Post Ischemia-Reperfusion.
In this study, we have shown that P played a critical role in the pathogenesis of aHUS in a murine model of the disease.
Title: Blocking Properdin Prevents Complement-Mediated Hemolytic Uremic Syndrome and Systemic Thrombophilia.
Properdin deficiency protects from 5-fluorouracil-induced small intestinal mucositis in a complement activation-independent, interleukin-10-dependent mechanism
Title: Properdin deficiency protects from 5-fluorouracil-induced small intestinal mucositis in a complement activation-independent, interleukin-10-dependent mechanism.
We induced anti-myeloperoxidase vasculitis in mice and showed that neither MASP-2- nor properdin-deficient mice were protected, suggesting that alternative pathway activation does not require properdin or the lectin pathway.
Title: Experimentally-induced anti-myeloperoxidase vasculitis does not require properdin, MASP-2 or bone marrow-derived C5.
The results show that Properdin plays a key role in allergen-induced airway inflammation and represents a potential therapeutic target for human asthma.
Title: Properdin Contributes to Allergic Airway Inflammation through Local C3a Generation.
Authors conclude that properdin controls the strength of immune responses by affecting humoral as well as cellular phenotypes during acute bacterial infection and ensuing inflammation.
Title: Septicaemia models using Streptococcus pneumoniae and Listeria monocytogenes: understanding the role of complement properdin.
Properdin deficiency exacerbated renal injury in mice lacking complement factor H.
Title: Loss of properdin exacerbates C3 glomerulopathy resulting from factor H deficiency.
deficiency of properdin in mice with factor H mutation exacerbates C3 glomerulonephritis
Title: Combination of factor H mutation and properdin deficiency causes severe C3 glomerulonephritis.

Submit: New GeneRIF Correction See all GeneRIFs (15)

Variation

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Alleles

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

Endonuclease-mediated (3)
Targeted (4) 1 citation

Interactions

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Products	Interactant	Other Gene	Complex	Source	Pubs	Description

General gene information

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Markers

AW822254 (e-PCR)
- UniSTS:209508

Cfp (e-PCR), detects polymorphism
- UniSTS:532667

NoName (e-PCR)
- UniSTS:490724

Gene Ontology Provided by MGI

Process	Evidence Code	Pubs
involved_in complement activation	NAS Non-traceable Author Statement more info	PubMed
involved_in complement activation, alternative pathway	IMP Inferred from Mutant Phenotype more info	PubMed
involved_in positive regulation of immune response	NAS Non-traceable Author Statement more info	PubMed
involved_in positive regulation of opsonization	NAS Non-traceable Author Statement more info	PubMed

Component	Evidence Code	Pubs
located_in cytoplasmic side of Golgi membrane	ISO Inferred from Sequence Orthology more info
located_in cytoplasmic side of Golgi membrane	NAS Non-traceable Author Statement more info	PubMed
located_in extracellular space	IDA Inferred from Direct Assay more info	PubMed
located_in secretory granule	IDA Inferred from Direct Assay more info	PubMed

General protein information

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Preferred Names: properdin

Names: complement factor P; properdin factor, complement

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.