Entry - *602592 - LYMPHOCYTE ANTIGEN CD5-LIKE; CD5L - OMIM
 
* 602592

LYMPHOCYTE ANTIGEN CD5-LIKE; CD5L


Alternative titles; symbols

SCAVENGER RECEPTOR CYSTEINE-RICH FAMILY, MEMBER SP-ALPHA
SP-ALPHA
APOPTOSIS INHIBITOR 6; API6
APOPTOSIS INHIBITOR OF MACROPHAGES; AIM


HGNC Approved Gene Symbol: CD5L

Cytogenetic location: 1q23.1     Genomic coordinates (GRCh38): 1:157,827,068-157,841,808 (from NCBI)


TEXT

Cloning and Expression

Scavenger receptor cysteine-rich (SRCR) family members are among the proteins that regulate leukocyte function. One group of SRCR proteins includes CD5 (153340) and CD6 (186720), both of which have 3 SRCR-like domains each containing 8 cysteine residues in their extracellular region, a hydrophobic transmembrane domain, and a long cytoplasmic domain. While searching for new SRCR family members in sequence databases, Gebe et al. (1997) identified a gene with extensive homology to CD5 and CD6. The predicted 347-amino acid protein, which they called Sp-alpha, has a 19-amino acid signal sequence followed by 3 cysteine-rich SRCR domains. Northern blot analysis detected 3 mRNAs of 2.4, 2.1, and 1.8 kb in spleen, lymph node, thymus, bone marrow, and fetal liver, but not in nonlymphoid tissues. Some resting myeloid cell lines, as well as peripheral blood monocytes, were capable of binding Sp-alpha.


Gene Function

Arai et al. (2005) found that Aim expression was induced in mouse macrophages in response to loading with highly oxidized low density lipoprotein (oxLDL), and that Aim was expressed in foam cells within atherosclerotic lesions. Both the expression of Aim in lesions and its induction by oxLDL required Lxr (see 602423)/Rxr (see 180245) heterodimers. Aim-null macrophages were highly susceptible to oxLDL-induced apoptosis in vitro and underwent accelerated apoptosis in atherosclerotic lesions in vivo. Double knockout of Aim and Ldlr (606945) reduced atherosclerotic lesions. Arai et al. (2005) concluded that AIM expression protects macrophages from apoptosis within atherosclerotic lesions, promoting early lesion development.


Mapping

Gebe et al. (1997) mapped the Sp-alpha gene to 1q21-q23 by fluorescence in situ hybridization.


REFERENCES

  1. Arai, S., Shelton, J. M., Chen, M., Bradley, M. N., Castrillo, A., Bookout, A. L., Mak, P. A., Edwards, P. A., Mangelsdorf, D. J., Tontonoz, P., Miyazaki, T. A role for the apoptosis inhibitory factor AIM/Sp-alpha/Api6 in atherosclerosis development. Cell Metab. 1: 201-213, 2005. [PubMed: 16054063, related citations] [Full Text]

  2. Gebe, J. A., Kiener, P. A., Ring, H. Z., Li, X., Francke, U., Aruffo, A. Molecular cloning, mapping to human chromosome 1 q21-q23, and cell binding characteristics of Sp-alpha, a new member of the scavenger receptor cysteine-rich (SRCR) family of proteins. J. Biol. Chem. 272: 6151-6158, 1997. [PubMed: 9045627, related citations] [Full Text]


Contributors:
Patricia A. Hartz - updated : 4/19/2005
Creation Date:
Rebekah S. Rasooly : 5/4/1998
mgross : 04/20/2005
terry : 4/19/2005
mgross : 1/12/2005
alopez : 5/8/1998
alopez : 5/4/1998

* 602592

LYMPHOCYTE ANTIGEN CD5-LIKE; CD5L


Alternative titles; symbols

SCAVENGER RECEPTOR CYSTEINE-RICH FAMILY, MEMBER SP-ALPHA
SP-ALPHA
APOPTOSIS INHIBITOR 6; API6
APOPTOSIS INHIBITOR OF MACROPHAGES; AIM


HGNC Approved Gene Symbol: CD5L

Cytogenetic location: 1q23.1     Genomic coordinates (GRCh38): 1:157,827,068-157,841,808 (from NCBI)


TEXT

Cloning and Expression

Scavenger receptor cysteine-rich (SRCR) family members are among the proteins that regulate leukocyte function. One group of SRCR proteins includes CD5 (153340) and CD6 (186720), both of which have 3 SRCR-like domains each containing 8 cysteine residues in their extracellular region, a hydrophobic transmembrane domain, and a long cytoplasmic domain. While searching for new SRCR family members in sequence databases, Gebe et al. (1997) identified a gene with extensive homology to CD5 and CD6. The predicted 347-amino acid protein, which they called Sp-alpha, has a 19-amino acid signal sequence followed by 3 cysteine-rich SRCR domains. Northern blot analysis detected 3 mRNAs of 2.4, 2.1, and 1.8 kb in spleen, lymph node, thymus, bone marrow, and fetal liver, but not in nonlymphoid tissues. Some resting myeloid cell lines, as well as peripheral blood monocytes, were capable of binding Sp-alpha.


Gene Function

Arai et al. (2005) found that Aim expression was induced in mouse macrophages in response to loading with highly oxidized low density lipoprotein (oxLDL), and that Aim was expressed in foam cells within atherosclerotic lesions. Both the expression of Aim in lesions and its induction by oxLDL required Lxr (see 602423)/Rxr (see 180245) heterodimers. Aim-null macrophages were highly susceptible to oxLDL-induced apoptosis in vitro and underwent accelerated apoptosis in atherosclerotic lesions in vivo. Double knockout of Aim and Ldlr (606945) reduced atherosclerotic lesions. Arai et al. (2005) concluded that AIM expression protects macrophages from apoptosis within atherosclerotic lesions, promoting early lesion development.


Mapping

Gebe et al. (1997) mapped the Sp-alpha gene to 1q21-q23 by fluorescence in situ hybridization.


REFERENCES

  1. Arai, S., Shelton, J. M., Chen, M., Bradley, M. N., Castrillo, A., Bookout, A. L., Mak, P. A., Edwards, P. A., Mangelsdorf, D. J., Tontonoz, P., Miyazaki, T. A role for the apoptosis inhibitory factor AIM/Sp-alpha/Api6 in atherosclerosis development. Cell Metab. 1: 201-213, 2005. [PubMed: 16054063] [Full Text: https://doi.org/10.1016/j.cmet.2005.02.002]

  2. Gebe, J. A., Kiener, P. A., Ring, H. Z., Li, X., Francke, U., Aruffo, A. Molecular cloning, mapping to human chromosome 1 q21-q23, and cell binding characteristics of Sp-alpha, a new member of the scavenger receptor cysteine-rich (SRCR) family of proteins. J. Biol. Chem. 272: 6151-6158, 1997. [PubMed: 9045627] [Full Text: https://doi.org/10.1074/jbc.272.10.6151]


Contributors:
Patricia A. Hartz - updated : 4/19/2005

Creation Date:
Rebekah S. Rasooly : 5/4/1998

Edit History:
mgross : 04/20/2005
terry : 4/19/2005
mgross : 1/12/2005
alopez : 5/8/1998
alopez : 5/4/1998