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• W2419084966 endingPage "e12812" @default.
• W2419084966 startingPage "e12812" @default.
• W2419084966 abstract "Systemic deficiency of PIKfyve, the evolutionarily conserved phosphoinositide kinase synthesizing cellular PtdIns5P and PtdIns(3,5)P2 and implicated in insulin signaling, causes early embryonic death in mice. In contrast, mice with muscle-specific Pikfyve disruption have normal lifespan but exhibit early-age whole-body glucose intolerance and muscle insulin resistance, thus establishing the key role of muscle PIKfyve in glucose homeostasis. Fat and muscle tissues control postprandial glucose clearance through different mechanisms, raising questions as to whether adipose Pikfyve disruption will also trigger whole-body metabolic abnormalities, and if so, what the mechanism might be. To clarify these issues, here we have characterized two new mouse models with adipose tissue disruption of Pikfyve through Cre recombinase expression driven by adipose-specific aP2- or adiponectin (Aq) promoters. Whereas both mouse lines were ostensibly normal until adulthood, their glucose homeostasis and systemic insulin sensitivity were severely dysregulated. These abnormalities stemmed in part from accelerated fat-cell lipolysis and elevated serum FFA. Intriguingly, aP2-Cre-PIKfyvefl/fl but not Aq-Cre-PIKfyvefl/fl females had severely impaired pregnancy-induced mammary gland differentiation and lactogenesis, consistent with aP2-Cre-mediated Pikfyve excision in nonadipogenic tissues underlying this defect. Intriguingly, whereas mammary glands from postpartum control and Aq-Cre-PIKfyvefl/fl mice or ex vivo mammary gland explants showed profound upregulation of PIKfyve protein levels subsequent to prolactin receptor activation, such increases were not apparent in aP2-Cre-PIKfyvefl/fl females. Collectively, our data identify for the first time that adipose tissue Pikfyve plays a key role in the mechanisms regulating glucose homeostasis and that the PIKfyve pathway is critical in mammary epithelial differentiation during pregnancy and lactogenesis downstream of prolactin receptor signaling." @default.
• W2419084966 created "2016-06-24" @default.
• W2419084966 creator A5023734904 @default.
• W2419084966 creator A5032477509 @default.
• W2419084966 creator A5057279048 @default.
• W2419084966 creator A5058886568 @default.
• W2419084966 creator A5068307980 @default.
• W2419084966 date "2016-06-01" @default.
• W2419084966 modified "2023-09-23" @default.
• W2419084966 title "Unexpected severe consequences of Pikfyve deletion by aP2- or Aq-promoter-driven Cre expression for glucose homeostasis and mammary gland development" @default.
• W2419084966 cites W1495521853 @default.
• W2419084966 cites W1541118885 @default.
• W2419084966 cites W1579001936 @default.
• W2419084966 cites W1878213572 @default.
• W2419084966 cites W1940950287 @default.
• W2419084966 cites W1964873147 @default.
• W2419084966 cites W1970036962 @default.
• W2419084966 cites W1975543728 @default.
• W2419084966 cites W1977341142 @default.
• W2419084966 cites W1978804351 @default.
• W2419084966 cites W1989283034 @default.
• W2419084966 cites W1994246367 @default.
• W2419084966 cites W1997048738 @default.
• W2419084966 cites W2004651360 @default.
• W2419084966 cites W2004861205 @default.
• W2419084966 cites W2012037560 @default.
• W2419084966 cites W2016108853 @default.
• W2419084966 cites W2016728909 @default.
• W2419084966 cites W2016941990 @default.
• W2419084966 cites W2022857776 @default.
• W2419084966 cites W2025891519 @default.
• W2419084966 cites W2026676056 @default.
• W2419084966 cites W2027474840 @default.
• W2419084966 cites W2029250190 @default.
• W2419084966 cites W2030721984 @default.
• W2419084966 cites W2032196335 @default.
• W2419084966 cites W2032462280 @default.
• W2419084966 cites W2034320996 @default.
• W2419084966 cites W2034408892 @default.
• W2419084966 cites W2035398977 @default.
• W2419084966 cites W2037985807 @default.
• W2419084966 cites W2039647519 @default.
• W2419084966 cites W2042283565 @default.
• W2419084966 cites W2047179833 @default.
• W2419084966 cites W2047984068 @default.
• W2419084966 cites W2050379370 @default.
• W2419084966 cites W2052908389 @default.
• W2419084966 cites W2066702528 @default.
• W2419084966 cites W2068382369 @default.
• W2419084966 cites W2072009619 @default.
• W2419084966 cites W2072107269 @default.
• W2419084966 cites W2073057670 @default.
• W2419084966 cites W2073578382 @default.
• W2419084966 cites W2078374645 @default.
• W2419084966 cites W2083634877 @default.
• W2419084966 cites W2085820610 @default.
• W2419084966 cites W2086250047 @default.
• W2419084966 cites W2091884933 @default.
• W2419084966 cites W2092328207 @default.
• W2419084966 cites W2093499847 @default.
• W2419084966 cites W2097278274 @default.
• W2419084966 cites W2097952652 @default.
• W2419084966 cites W2099132477 @default.
• W2419084966 cites W2102364504 @default.
• W2419084966 cites W2103370215 @default.
• W2419084966 cites W2105178322 @default.
• W2419084966 cites W2106959576 @default.
• W2419084966 cites W2109356083 @default.
• W2419084966 cites W2113366942 @default.
• W2419084966 cites W2117468155 @default.
• W2419084966 cites W2121795850 @default.
• W2419084966 cites W2124455076 @default.
• W2419084966 cites W2125709881 @default.
• W2419084966 cites W2128368215 @default.
• W2419084966 cites W2142979249 @default.
• W2419084966 cites W2146061561 @default.
• W2419084966 cites W2146193579 @default.
• W2419084966 cites W2146414563 @default.
• W2419084966 cites W2147028876 @default.
• W2419084966 cites W2149494884 @default.
• W2419084966 cites W2150232019 @default.
• W2419084966 cites W2152826474 @default.
• W2419084966 cites W2156840496 @default.
• W2419084966 cites W2160940105 @default.
• W2419084966 cites W2162228329 @default.
• W2419084966 cites W2166487029 @default.
• W2419084966 cites W2168761911 @default.
• W2419084966 cites W2171290692 @default.
• W2419084966 cites W2197315621 @default.
• W2419084966 cites W2318847305 @default.
• W2419084966 cites W2412231859 @default.
• W2419084966 cites W2430143578 @default.
• W2419084966 doi "https://doi.org/10.14814/phy2.12812" @default.
• W2419084966 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4908490" @default.
• W2419084966 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/27273882" @default.
• W2419084966 hasPublicationYear "2016" @default.
• W2419084966 type Work @default.
• W2419084966 sameAs 2419084966 @default.

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