IndraLab

Statements

KCNH3 activates cell population proliferation. 10 / 10
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"In contrast, loss of BEC-1 function further decreased germ cell proliferation in the glp-1 (e2141lf) loss of function allele (XREF_SUPPLEMENTARY), which is characterized by a reduction in germline progenitors, and a severe Glp (Germline abnormal proliferation) phenotype, where germ cells do not proliferate and differentiate prematurely [XREF_BIBR]."
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"Taken together, our glp-1 and Notch gain and loss of function experiments suggest that BEC-1 and Beclin1 functions, at least in part, independently of GLP-1 and Notch activity to promote germ cell proliferation."
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"BEC-1 functions in a DAF-18 and PTEN and SKN-1 and Nrf dependent but DAF-16 and FOXO independent manner to promote germline proliferation."
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"BEC-1 and Beclin1 promotes germline stem cell proliferation cell non autonomously from somatic tissues."
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"We further show that BEC-1 and Beclin1 acts independently of the GLP-1 and Notch or DAF-7 and TGFbeta pathways, but together with the DAF-2 and insulin IGF-1 receptor (IIR) signaling pathway to promote germline stem cell proliferation."
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"For example, ATG-16.2/ATG16L and ATG-18/WIPI1/2 require the DAF-16 and FOXO transcription factor, and the phosphatase and tensin homolog DAF-18 and PTEN, whereas BEC-1 activity is dependent on DAF-18 and PTEN and SKN-1 and Nrf (nuclear-factorerythroid-related factor), but independent of the DAF-16 and FOXO transcription factor to promote germline proliferation."
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"We conclude that bec-1 acts in a pathway with daf-2 and IIR signaling to promote germline proliferation."
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"We found that BEC-1 expression from a hypodermal [Pdpy-7 : : BEC-1], a muscle specific [Pmyo-3 : : BEC-1], its own promoter [Pbec-1 : : BEC-1], and less so from a pan-neuronal promoter [Prgef-1 : : BEC-1], rescued the germline proliferation defects in bec-1 mutant animals (XREF_FIG, XREF_SUPPLEMENTARY)."
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"In contrast, expression of bec-1 from an intestinal promoter [Pglo-1 : : BEC-1] did not rescue the proliferation defect of bec-1 mutants (XREF_FIG)."
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"In vitro studies showed that KCNH3 silencing in OC cells could inhibit cell proliferation and migration ability, and induce apoptosis and G2/M phase arrest."
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