IndraLab

Statements

CACNA1G inhibits cell population proliferation. 10 / 11
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"Although we observed that the pharmaceutical inhibition of CaV3.1 decreased differentiation, where adipogenesis is associated with enhanced Ca influx (Zhang et al. 2018), inhibition of CaV3.1 actually augmented proliferation."
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"Besides, increased G1 and decreased S proportions plus decreased, CCND1, a key protein in G1/S checkpoint, indicated that constrained G1/S transition may contribute to the molecular mechanism for CAV3.1 knockdown induced proliferation in PCa."
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"Having said that, CACNA1G silencing enhanced proliferation of MCF-7 cells as compared to CACNA1H silencing [38]."
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"Notably, CACNA1G gene knock-down and the Ca V 3 channel blocker, mibefradil, significantly reduced the rate of cell proliferation in this cancer [XREF_BIBR]."
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"Importantly, ectopic expression of Akt rescued the most inhibitory effects on proliferation and invasion induced by CAV3.1 knockdown in PCa."
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"(p71) In glioblastoma, inhibiting CaV3.1 disrupts autophagy, suppressing cell proliferation and improving resistance to temozolomide chemotherapy."
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"In human glioblastoma cells, mibefradil, a T-type Ca 2+ channel blocker with a weak L-type channel inhibiting activity [XREF_BIBR], and siRNA mediated downregulation of CACNA1G (Ca V.3.1) and CACNA1H (Ca V 3.2) reduces cell proliferation, induces apoptotic cell death, and sensitizes cells to ionizing radiation via AKT and mTORC2 axis [XREF_BIBR]."
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"Human pulmonary artery myocytes express CaV3.1 and silencing of CaV3.1 inhibits serum-induced proliferation [25]."
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"Knockdown of CaV3.1 indeed induces cell proliferation and reduces apoptosis in MCF-7 breast cancer cells."
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"The Cav3.1 null mice impaired the proliferation and differentiation of the neuro-progenitor cells."
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