CCL3L1

Chemokine (C-C motif) ligand 3-like 1

PDB rendering based on 1b50.
Identifiers
Symbols CCL3L1; 464.2; D17S1718; G0S19-2; LD78; LD78BETA; MGC104178; MGC12815; MGC182017; MIP1AP; SCYA3L; SCYA3L1
External IDs OMIM: 601395 MGI: 98260 HomoloGene: 2242 GeneCards: CCL3L1 Gene
Orthologs
Species Human Mouse
Entrez 6349 20302
Ensembl n/a ENSMUSG00000000982
UniProt P16619 Q3U6F9
RefSeq (mRNA) NM_021006 NM_011337.2
RefSeq (protein) NP_066286 NP_035467.1
Location (UCSC) n/a Chr 11:
83.46 – 83.46 Mb
PubMed search [1] [2]

Chemokine (C-C motif) ligand 3-like 1, also known as CCL3L1, is a protein which in humans is encoded by the CCL3L1 gene.[1][2][3]

Contents

Function

This gene is one of several chemokine genes clustered on the q-arm of chromosome 17. Chemokines are a family of secreted proteins involved in immunoregulatory and inflammatory processes. Specifically, chemokines attract lymphocytes to sites of infection or damage. This protein binds to several chemokine receptors including chemokine binding protein 2 (CCBP2 or D6) and chemokine (C-C motif) receptor 5 (CCR5).

CCR5 is a co-receptor for HIV, and binding of CCL3L1 to CCR5 inhibits HIV entry. Furthermore, the binding causes the receptor to be taken inside the cell by endocytosis, to eventually be reprocessed and re-expressed.[1]

Gene organization

The human genome reference assembly contains two full copies of the gene (CCL3L1 and CCL3L3) and an additional partial duplication, which is thought to result in a pseudogene, designated CCL3L2. This record represents the more telomeric full-length gene.[1]

Clinical significance

The copy number of this gene varies among individuals. This is hypothesized to be due to segmental duplication of the region containing CCL3. Most individuals have 1-6 copies in the diploid genome, although rare individuals have zero or more than six copies. With increased copy number, there is more CCL3L1 expressed, and so competition for the CCR5 binding site is increased. This leads to slower advancement of disease in HIV-infected individuals, giving those with greater copy number more resistance.[1]

Interactions

CCL3L1 has been shown to interact with CCR5.[4][5]

References

  1. ^ a b c d "Entrez Gene: CCL3L1 chemokine (C-C motif) ligand 3-like 1". http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=6349. 
  2. ^ Irving SG, Zipfel PF, Balke J, McBride OW, Morton CC, Burd PR, Siebenlist U, Kelly K (June 1990). "Two inflammatory mediator cytokine genes are closely linked and variably amplified on chromosome 17q". Nucleic Acids Res. 18 (11): 3261–70. doi:10.1093/nar/18.11.3261. PMC 330932. PMID 1972563. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=330932. 
  3. ^ Hirashima M, Ono T, Nakao M, Nishi H, Kimura A, Nomiyama H, Hamada F, Yoshida MC, Shimada K (1992). "Nucleotide sequence of the third cytokine LD78 gene and mapping of all three LD78 gene loci to human chromosome 17". DNA Seq. 3 (4): 203–12. doi:10.3109/10425179209034019. PMID 1296815. 
  4. ^ Miyakawa, Toshikazu; Obaru Kenshi, Maeda Kenji, Harada Shigeyoshi, Mitsuya Hiroaki (Feb. 2002). "Identification of amino acid residues critical for LD78beta, a variant of human macrophage inflammatory protein-1alpha, binding to CCR5 and inhibition of R5 human immunodeficiency virus type 1 replication". J. Biol. Chem. (United States) 277 (7): 4649–55. doi:10.1074/jbc.M109198200. ISSN 0021-9258. PMID 11734558. 
  5. ^ Struyf, S; Menten P, Lenaerts J P, Put W, D'Haese A, De Clercq E, Schols D, Proost P, Van Damme J (Jul. 2001). "Diverging binding capacities of natural LD78beta isoforms of macrophage inflammatory protein-1alpha to the CC chemokine receptors 1, 3 and 5 affect their anti-HIV-1 activity and chemotactic potencies for neutrophils and eosinophils". Eur. J. Immunol. (Germany) 31 (7): 2170–8. doi:10.1002/1521-4141(200107)31:7<2170::AID-IMMU2170>3.0.CO;2-D. ISSN 0014-2980. PMID 11449371. 

Further reading