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• W2118946369 startingPage "167" @default.
• W2118946369 abstract "Summary WNT1 and WNT3a have been described as having redundant roles in promoting the development of neural crest‐derived melanocytes (NC‐Ms). We used cell lineage restricted retroviral infections to examine the effects of WNT signaling on defined cell types in neural crest cultures. RCAS retroviral infections were targeted to melanoblasts (NC‐M precursor cells) derived from transgenic mice that express the virus receptor, TVA, under the control of a melanoblast promoter (DCT). As expected, over 90% of DCT–TVA+ cells expressed early melanoblast markers MITF and KIT. However, by following the fate of infected cells in standard culture conditions, we find that only 5% of descendents were NC‐Ms. The majority of the descendents were not NC‐Ms, but expressed smooth muscle cell markers, demonstrating that mammalian melanoblasts are not committed to the NC‐M lineage. RCAS infection of DCT–TVA+ cells demonstrated that overexpression of canonical WNT signaling genes ( β CAT, WNT3a or WNT1) can increase NC‐M numbers in an endothelin dependent manner. However, WNT1 and WNT3a have different modes of action with respect to melanoblast fate. Intrinsic over‐expression of β CAT or WNT3a can increase NC‐M numbers by biasing the fate of DCT–TVA+ cells to NC‐Ms. In contrast, the DCT–TVA+ melanoblasts cannot respond to WNT1 signaling and do not alter their fate towards NC‐M. Instead, WNT1 only increases NC‐M numbers through paracrine signaling on melanoblast precursors to increase the numbers of neural crest cells that become NC‐Ms." @default.
• W2118946369 created "2016-06-24" @default.
• W2118946369 creator A5007492882 @default.
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• W2118946369 creator A5062604430 @default.
• W2118946369 creator A5080193192 @default.
• W2118946369 creator A5089723549 @default.
• W2118946369 date "2005-04-22" @default.
• W2118946369 modified "2023-10-16" @default.
• W2118946369 title "WNT1 and WNT3a promote expansion of melanocytes through distinct modes of action" @default.
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• W2118946369 cites W1559850800 @default.
• W2118946369 cites W1576536426 @default.
• W2118946369 cites W1667206495 @default.
• W2118946369 cites W1854163003 @default.
• W2118946369 cites W1924380893 @default.
• W2118946369 cites W1928152403 @default.
• W2118946369 cites W1963091570 @default.
• W2118946369 cites W1963652662 @default.
• W2118946369 cites W1964079625 @default.
• W2118946369 cites W1965088658 @default.
• W2118946369 cites W1965824208 @default.
• W2118946369 cites W1971239441 @default.
• W2118946369 cites W1973497708 @default.
• W2118946369 cites W1985403883 @default.
• W2118946369 cites W1987047126 @default.
• W2118946369 cites W1993781672 @default.
• W2118946369 cites W1995305478 @default.
• W2118946369 cites W1997889534 @default.
• W2118946369 cites W1998291423 @default.
• W2118946369 cites W2000146676 @default.
• W2118946369 cites W2010684135 @default.
• W2118946369 cites W2014329049 @default.
• W2118946369 cites W2015964634 @default.
• W2118946369 cites W2018876009 @default.
• W2118946369 cites W2019668010 @default.
• W2118946369 cites W2020830179 @default.
• W2118946369 cites W2023009035 @default.
• W2118946369 cites W2023186669 @default.
• W2118946369 cites W2026321840 @default.
• W2118946369 cites W2030940111 @default.
• W2118946369 cites W2033032651 @default.
• W2118946369 cites W2035059684 @default.
• W2118946369 cites W2040098499 @default.
• W2118946369 cites W2041795984 @default.
• W2118946369 cites W2042193781 @default.
• W2118946369 cites W2044910712 @default.
• W2118946369 cites W2051718122 @default.
• W2118946369 cites W2054237263 @default.
• W2118946369 cites W2055972315 @default.
• W2118946369 cites W2057099402 @default.
• W2118946369 cites W2059979526 @default.
• W2118946369 cites W2060209491 @default.
• W2118946369 cites W2061313029 @default.
• W2118946369 cites W2062595374 @default.
• W2118946369 cites W2069389397 @default.
• W2118946369 cites W2077406721 @default.
• W2118946369 cites W2078002199 @default.
• W2118946369 cites W2081853773 @default.
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• W2118946369 cites W2087431503 @default.
• W2118946369 cites W2095107795 @default.
• W2118946369 cites W2097419698 @default.
• W2118946369 cites W2100388117 @default.
• W2118946369 cites W2105516543 @default.
• W2118946369 cites W2107006976 @default.
• W2118946369 cites W2116227695 @default.
• W2118946369 cites W2119239047 @default.
• W2118946369 cites W2121653039 @default.
• W2118946369 cites W2125882882 @default.
• W2118946369 cites W2129475606 @default.
• W2118946369 cites W2130987003 @default.
• W2118946369 cites W2135142758 @default.
• W2118946369 cites W2138143482 @default.
• W2118946369 cites W2145402938 @default.
• W2118946369 cites W2146384126 @default.
• W2118946369 cites W2147257521 @default.
• W2118946369 cites W2150295764 @default.
• W2118946369 cites W2154041910 @default.
• W2118946369 cites W2159299286 @default.
• W2118946369 cites W2159522663 @default.
• W2118946369 cites W2160776258 @default.
• W2118946369 cites W2161073961 @default.
• W2118946369 cites W2162497387 @default.
• W2118946369 cites W2164927488 @default.
• W2118946369 cites W2170433626 @default.
• W2118946369 cites W2170650848 @default.
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• W2118946369 doi "https://doi.org/10.1111/j.1600-0749.2005.00226.x" @default.
• W2118946369 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/15892713" @default.
• W2118946369 hasPublicationYear "2005" @default.
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