Disease relevance of CACNA1G

• Aberrant methylation of CACNA1G was also examined in various human primary tumors and was detected in 17 of 49 (35%) colorectal cancers, 4 of 16 (25%) gastric cancers, and 3 of 23 (13%) acute myelogenous leukemia cases [1].

High impact information on CACNA1G

• Inactivation of CACNA1G, a T-type calcium channel gene, by aberrant methylation of its 5' CpG island in human tumors [1].
• By reverse transcriptase-PCR we detected expression of CACNA1G in normal colon and bone marrow, but expression was absent in the five tumor cell lines in which methylation was found [1].
• Inactivation of CACNA1G may play a role in cancer development by modulating calcium signaling, which potentially affects cell proliferation and apoptosis [1].
• To understand how the decrease in expression is linked to cell differentiation, we examined transcriptional regulation of the Cav3.1 Ca channel gene, CACNA1G [2].
• Alternative splicing of CACNA1G RNA may lead to expression of as many as 24 distinct protein products, ranging from 2171 to 2377 amino-acids residues [3].

Biological context of CACNA1G

• After treatment with the methylation inhibitor 5-deoxyazacytidine, the expression of CACNA1G was restored in all five cell lines [1].

Other interactions of CACNA1G

• We then used this fragment to screen human heart and rat brain lambda gt10 libraries, leading to the cloning of two full-length cDNAs derived from distinct genes (CACNA1G and CACNA1H) [4].
• The structure of CACNA1G, the gene encoding alpha1G, a human brain T Ca2+ channel alpha1 subunit, was determined by comparison of polymerase chain reaction-amplified brain cDNA and genomic sequences [3].

References