FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2484808876> ?p ?o ?g. }

• W2484808876 endingPage "839" @default.
• W2484808876 startingPage "829" @default.
• W2484808876 abstract "E2F transcription factors are important regulators of the cell cycle, and unrestrained activation of E2F-dependent transcription is considered to be an important driver of tumor formation and progression. Although highly expressed in normal skin and skin cancer, the role of the atypical E2Fs, E2F7 and E2F8, in keratinocyte homeostasis, regeneration and tumorigenesis is unknown. Surprisingly, keratinocyte-specific deletion of E2F7 and E2F8 in mice did not interfere with skin development and wound healing. However, the rate for successful isolation and establishment of E2f7/8-deficient primary keratinocyte cultures was much higher than for wild-type keratinocytes. Moreover, E2f7/8-deficient primary keratinocytes proliferate more efficiently under stress conditions, such as low/high confluence or DNA damage. Application of in vivo stress using the DMBA/TPA skin carcinogenesis protocol revealed that combined inactivation of E2f7/8 enhanced tumorigenesis and accelerated malignant progression. Loss of atypical E2Fs resulted in increased expression of E2F target genes, including E2f1. Additional loss of E2f1 did not rescue, but worsened skin tumorigenesis. We show that loss of E2F7/8 triggers apoptosis via induction of E2F1 in response to stress, indicating that the tumor-promoting effect of E2F7/8 inactivation can be partially compensated via E2F1-dependent apoptosis. Importantly, E2F7/8 repressed a large set of E2F target genes that are highly expressed in human patients with skin cancer. Together, our studies demonstrate that atypical E2Fs act as tumor suppressors, most likely via transcriptional repression of cell cycle genes in response to stress." @default.
• W2484808876 created "2016-08-23" @default.
• W2484808876 creator A5001349587 @default.
• W2484808876 creator A5010696819 @default.
• W2484808876 creator A5018221488 @default.
• W2484808876 creator A5020772605 @default.
• W2484808876 creator A5033711163 @default.
• W2484808876 creator A5061182628 @default.
• W2484808876 creator A5072399801 @default.
• W2484808876 creator A5073571156 @default.
• W2484808876 creator A5080303888 @default.
• W2484808876 creator A5082394976 @default.
• W2484808876 creator A5090532083 @default.
• W2484808876 date "2016-07-25" @default.
• W2484808876 modified "2023-10-06" @default.
• W2484808876 title "Synergistic functions of E2F7 and E2F8 are critical to suppress stress-induced skin cancer" @default.
• W2484808876 cites W1522395468 @default.
• W2484808876 cites W1577577364 @default.
• W2484808876 cites W1885235228 @default.
• W2484808876 cites W1982039056 @default.
• W2484808876 cites W1984252723 @default.
• W2484808876 cites W2001627329 @default.
• W2484808876 cites W2004042953 @default.
• W2484808876 cites W2005011918 @default.
• W2484808876 cites W2009527263 @default.
• W2484808876 cites W2019562165 @default.
• W2484808876 cites W2020288787 @default.
• W2484808876 cites W2020459118 @default.
• W2484808876 cites W2021744259 @default.
• W2484808876 cites W2023283617 @default.
• W2484808876 cites W2030974349 @default.
• W2484808876 cites W2035992391 @default.
• W2484808876 cites W2036561487 @default.
• W2484808876 cites W2038484987 @default.
• W2484808876 cites W2051907464 @default.
• W2484808876 cites W2055162988 @default.
• W2484808876 cites W2055917628 @default.
• W2484808876 cites W2057113047 @default.
• W2484808876 cites W2064113174 @default.
• W2484808876 cites W2064281414 @default.
• W2484808876 cites W2066143060 @default.
• W2484808876 cites W2068278990 @default.
• W2484808876 cites W2071311021 @default.
• W2484808876 cites W2096719176 @default.
• W2484808876 cites W2104049033 @default.
• W2484808876 cites W2104713031 @default.
• W2484808876 cites W2111346575 @default.
• W2484808876 cites W2116738722 @default.
• W2484808876 cites W2117692326 @default.
• W2484808876 cites W2121236039 @default.
• W2484808876 cites W2121271487 @default.
• W2484808876 cites W2121371748 @default.
• W2484808876 cites W2122511750 @default.
• W2484808876 cites W2134597949 @default.
• W2484808876 cites W2137509599 @default.
• W2484808876 cites W2140037284 @default.
• W2484808876 cites W2140522709 @default.
• W2484808876 cites W2142982089 @default.
• W2484808876 cites W2158217645 @default.
• W2484808876 cites W2164721923 @default.
• W2484808876 cites W2166374178 @default.
• W2484808876 cites W2167279371 @default.
• W2484808876 cites W2172194086 @default.
• W2484808876 cites W2289208429 @default.
• W2484808876 cites W2335175983 @default.
• W2484808876 doi "https://doi.org/10.1038/onc.2016.251" @default.
• W2484808876 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5311251" @default.
• W2484808876 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/27452520" @default.
• W2484808876 hasPublicationYear "2016" @default.
• W2484808876 type Work @default.
• W2484808876 sameAs 2484808876 @default.
• W2484808876 citedByCount "42" @default.
• W2484808876 countsByYear W24848088762017 @default.
• W2484808876 countsByYear W24848088762018 @default.
• W2484808876 countsByYear W24848088762019 @default.
• W2484808876 countsByYear W24848088762020 @default.
• W2484808876 countsByYear W24848088762021 @default.
• W2484808876 countsByYear W24848088762022 @default.
• W2484808876 countsByYear W24848088762023 @default.
• W2484808876 crossrefType "journal-article" @default.
• W2484808876 hasAuthorship W2484808876A5001349587 @default.
• W2484808876 hasAuthorship W2484808876A5010696819 @default.
• W2484808876 hasAuthorship W2484808876A5018221488 @default.
• W2484808876 hasAuthorship W2484808876A5020772605 @default.
• W2484808876 hasAuthorship W2484808876A5033711163 @default.
• W2484808876 hasAuthorship W2484808876A5061182628 @default.
• W2484808876 hasAuthorship W2484808876A5072399801 @default.
• W2484808876 hasAuthorship W2484808876A5073571156 @default.
• W2484808876 hasAuthorship W2484808876A5080303888 @default.
• W2484808876 hasAuthorship W2484808876A5082394976 @default.
• W2484808876 hasAuthorship W2484808876A5090532083 @default.
• W2484808876 hasBestOaLocation W24848088761 @default.
• W2484808876 hasConcept C104317684 @default.
• W2484808876 hasConcept C121608353 @default.
• W2484808876 hasConcept C183022183 @default.
• W2484808876 hasConcept C203014093 @default.
• W2484808876 hasConcept C2777074287 @default.
• W2484808876 hasConcept C29537977 @default.

• next