MSR1

Macrophage scavenger receptor 1, also known as MSR1, is a protein which in humans is encoded by the MSR1 gene.[5][6] MSR1 has also been designated CD204 (cluster of differentiation 204).

MSR1
Identifiers
AliasesMSR1, CD204, SCARA1, SR-A, SRA, phSR1, phSR2, macrophage scavenger receptor 1, SR-AI, SR-AII, SR-AIII
External IDsOMIM: 153622 MGI: 98257 HomoloGene: 12822 GeneCards: MSR1
Gene location (Human)
Chr.Chromosome 8 (human)[1]
Band8p22Start16,107,878 bp[1]
End16,567,490 bp[1]
RNA expression pattern




More reference expression data
Orthologs
SpeciesHumanMouse
Entrez

4481

20288

Ensembl

ENSG00000038945

ENSMUSG00000025044

UniProt

P21757

P30204

RefSeq (mRNA)

NM_138716
NM_002445
NM_138715
NM_001363744

NM_001113326
NM_031195

RefSeq (protein)

NP_002436
NP_619729
NP_619730
NP_001350673

NP_001106797
NP_112472

Location (UCSC)Chr 8: 16.11 – 16.57 MbChr 8: 39.58 – 39.64 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

Function

This gene encodes the class A macrophage scavenger receptors, which include three different types (1, 2, 3) generated by alternative splicing of this gene. These receptors or isoforms are trimeric integral membrane glycoproteins and have been implicated in many macrophage-associated physiological and pathological processes including atherosclerosis, Alzheimer's disease, and host defense. They were thought to be expressed macrophage-specific, but recently shown to be present on different dendritic cells classes, too.[7]

The isoforms type 1 and type 2 are functional receptors and are able to mediate the endocytosis of modified low density lipoproteins (LDLs). The isoform type 3 does not internalize modified LDL (acetyl-LDL) despite having the domain shown to mediate this function in the types 1 and 2 isoforms. It has an altered intracellular processing and is trapped within the endoplasmic reticulum, making it unable to perform endocytosis. The isoform type 3 can inhibit the function of isoforms type 1 and type 2 when co-expressed, indicating a dominant negative effect and suggesting a mechanism for regulation of scavenger receptor activity in macrophages.[5]

Biotechnology application

Macrophage scavenger receptor has been shown to mediate adhesion of macrophages and other cell lines to tissue culture plastic.[8]

Interactions

MSR1 has been shown to interact with HSPA1A.[9]

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References

  1. GRCh38: Ensembl release 89: ENSG00000038945 - Ensembl, May 2017
  2. GRCm38: Ensembl release 89: ENSMUSG00000025044 - Ensembl, May 2017
  3. "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. "Entrez Gene: MSR1 macrophage scavenger receptor 1".
  6. Matsumoto A, Naito M, Itakura H, Ikemoto S, Asaoka H, Hayakawa I, Kanamori H, Aburatani H, Takaku F, Suzuki H (December 1990). "Human macrophage scavenger receptors: primary structure, expression, and localization in atherosclerotic lesions". Proc. Natl. Acad. Sci. U.S.A. 87 (23): 9133–7. Bibcode:1990PNAS...87.9133M. doi:10.1073/pnas.87.23.9133. PMC 55118. PMID 2251254.
  7. Herber DL, Cao W, Nefedova Y, Novitskiy SV, Nagaraj S, Tyurin VA, Corzo A, Cho HI, Celis E, Lennox B, Knight SC, Padhya T, McCaffrey TV, McCaffrey JC, Antonia S, Fishman M, Ferris RL, Kagan VE, Gabrilovich DI (August 2010). "Lipid accumulation and dendritic cell dysfunction in cancer". Nat. Med. 16 (8): 880–6. doi:10.1038/nm.2172. PMC 2917488. PMID 20622859.
  8. Robbins AK, Horlick RA (August 1998). "Macrophage scavenger receptor confers an adherent phenotype to cells in culture". BioTechniques. 25 (2): 240–4. PMID 9714883.
  9. Nakamura, Toshinobu; Hinagata Jun-ichi; Tanaka Toshiki; Imanishi Takeshi; Wada Youichiro; Kodama Tatsuhiko; Doi Takefumi (Jan 2002). "HSP90, HSP70, and GAPDH directly interact with the cytoplasmic domain of macrophage scavenger receptors". Biochem. Biophys. Res. Commun. United States. 290 (2): 858–64. doi:10.1006/bbrc.2001.6271. ISSN 0006-291X. PMID 11785981.

Further reading

This article incorporates text from the United States National Library of Medicine, which is in the public domain.

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