Alternative titles; symbols
HGNC Approved Gene Symbol: HSPB7
Cytogenetic location: 1p36.13 Genomic coordinates (GRCh38): 1:16,014,029-16,019,594 (from NCBI)
By searching an EST database for genes highly expressed in heart, Krief et al. (1999) identified 3 splice variants of HSPB7, which they called CVHSP. The major transcript encodes a deduced 170-amino acid protein with features of a small heat-shock protein, including an HSP20 (HSPB8; 608014) protein family motif and a conserved C-terminal domain. The minor CVHSP splice variants encode proteins of 175 and 68 amino acids. Northern blot analysis detected a major transcript of 2.3 kb and minor transcripts of 1.2 and 1.6 kb in heart and skeletal muscle. RNA dot blot analysis detected high expression of CVHSP in adult and fetal heart and in skeletal muscle, with weaker expression in aorta. RT-PCR showed CVHSP expression in adipose as well. Western blot analysis detected a major 25-kD CVHSP protein and a less abundant 23-kD protein.
Krief et al. (1999) determined that the HSPB7 gene contains at least 5 exons.
By genomic sequence analysis, Krief et al. (1999) mapped the HSPB7 gene to chromosome 1p36.23-p34.3.
By genomic sequence analysis, Naderi (2018) determined that the HSPB7 gene maps to chromosome 1p36.13, about 5.2 kb from the SRARP gene (619448) in a tail-to-tail orientation.
Using rat models of cardiac pathologies, Krief et al. (1999) found that Cvhsp mRNA expression in heart was unchanged in spontaneous hypertension, upregulated in right ventricular hypertrophy, and downregulated in left ventricular hypertrophy. In obese Zucker rats, Cvhsp mRNA was increased in skeletal muscle and in brown and white adipose tissue, but it was unchanged in heart. Yeast 2-hybrid analysis of a mouse embryo cDNA library and immunoprecipitation experiments using human heart homogenates showed that CVHSP interacted with alpha-filamin (FLNA; 300017).
By database analysis, Naderi (2018) found that SRARP and HSPB7 had closely correlated copy numbers across malignancies of multiple tissue origins. Epigenetic silencing appeared to regulate SRARP and HSPB7 expression across tumors and cancer cell lines of multiple tissue origins. SRARP and HSPB7 functioned as tumor suppressors and were widely deleted in malignancies of multiple tissue origins. Further investigation suggested that genomic and epigenetic alterations of SRARP and HSPB7 could predict cancer survival.
Krief, S., Faivre, J.-F., Robert, P., Le Douarin, B., Brument-Larignon, N., Lefrere, I., Bouzyk, M. M., Anderson, K. M., Greller, L. D., Tobin, F. L., Souchet, M., Bril, A. Identification and characterization of cvHsp: a novel human small stress protein selectively expressed in cardiovascular and insulin-sensitive tissues. J. Biol. Chem. 274: 36592-36600, 1999. [PubMed: 10593960] [Full Text: https://doi.org/10.1074/jbc.274.51.36592]
Naderi, A. SRARP and HSPB7 are epigenetically regulated gene pairs that function as tumor suppressors and predict clinical outcome in malignancies. Molec. Oncol. 12: 724-755, 2018. [PubMed: 29577611] [Full Text: https://doi.org/10.1002/1878-0261.12195]