FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2031570299> ?p ?o ?g. }

• W2031570299 endingPage "3421" @default.
• W2031570299 startingPage "3414" @default.
• W2031570299 abstract "The proto-oncogene c-myc has been shown to play a pivotal role in cell cycle regulation, metabolism, apoptosis, differentiation, cell adhesion, and tumorigenesis, and participates in regulating hematopoietic homeostasis. It is a transcription regulator that is part of an extensive network of interacting factors. Most probably, different biological responses are elicited by different overlapping subsets of c-Myc target genes, both induced and suppressed. Results obtained from studies employing mouse models are consistent with the need for at least one, and possibly two, mutations in addition to deregulated c-myc for malignant tumor formation. Repression of c-myc is required for terminal differentiation of many cell types, including hematopoietic cells. It has been shown that deregulated expression of c-myc in both M1 myeloid leukemic cells and normal myeloid cells derived from murine bone marrow, not only blocked terminal differentiation and its associated growth arrest, but also induced apoptosis, which is dependent on the Fas/CD95 pathway. There is evidence to suggest that the CD95/Fas death receptor pathway is an integral part of the apoptotic response associated with the end of the normal terminal myeloid differentiation program, and that deregulated c-myc expression can activate this signaling pathway prematurely. The ability of egr-1 to promote terminal myeloid differentiation when co-expressed with c-myc, and of c-fos to partially abrogate the block imparted by deregulated c-myc on myeloid differentiation, make these two genes candidate tumor suppressors. Several different transcription factors have been implicated in the down-regulation of c-myc expression during differentiation, including C/EBPalpha, CTCF, BLIMP-1, and RFX1. Alterations in the expression and/or function of these transcription factors, or of the c-Myc and Max interacting proteins, such as MM-1 and Mxi1, can influence the neoplastic process. Understanding how c-Myc controls cellular phenotypes, including the leukemic phenotype, should provide novel tools for designing drugs to promote differentiation and/or apoptosis of leukemic cells." @default.
• W2031570299 created "2016-06-24" @default.
• W2031570299 creator A5000040305 @default.
• W2031570299 creator A5043232744 @default.
• W2031570299 creator A5064200118 @default.
• W2031570299 creator A5068232329 @default.
• W2031570299 date "2002-05-13" @default.
• W2031570299 modified "2023-10-17" @default.
• W2031570299 title "The proto-oncogene c-myc in hematopoietic development and leukemogenesis" @default.
• W2031570299 cites W137827881 @default.
• W2031570299 cites W1502418486 @default.
• W2031570299 cites W1560485148 @default.
• W2031570299 cites W1599701369 @default.
• W2031570299 cites W1673934352 @default.
• W2031570299 cites W1838164985 @default.
• W2031570299 cites W1966951079 @default.
• W2031570299 cites W1967007700 @default.
• W2031570299 cites W1969413206 @default.
• W2031570299 cites W1971993554 @default.
• W2031570299 cites W1974852358 @default.
• W2031570299 cites W1984164498 @default.
• W2031570299 cites W1984903030 @default.
• W2031570299 cites W1987598864 @default.
• W2031570299 cites W1993004730 @default.
• W2031570299 cites W1993033800 @default.
• W2031570299 cites W2002423027 @default.
• W2031570299 cites W2004205790 @default.
• W2031570299 cites W2005393972 @default.
• W2031570299 cites W2008472774 @default.
• W2031570299 cites W2009603041 @default.
• W2031570299 cites W2010041535 @default.
• W2031570299 cites W2014624348 @default.
• W2031570299 cites W2016011359 @default.
• W2031570299 cites W2016567695 @default.
• W2031570299 cites W2021033472 @default.
• W2031570299 cites W2025438239 @default.
• W2031570299 cites W2026731083 @default.
• W2031570299 cites W2030844021 @default.
• W2031570299 cites W2033384486 @default.
• W2031570299 cites W2034769760 @default.
• W2031570299 cites W2034851913 @default.
• W2031570299 cites W2043541247 @default.
• W2031570299 cites W2044915747 @default.
• W2031570299 cites W2060696024 @default.
• W2031570299 cites W2061054054 @default.
• W2031570299 cites W2061494834 @default.
• W2031570299 cites W2063135487 @default.
• W2031570299 cites W2064772366 @default.
• W2031570299 cites W2068499309 @default.
• W2031570299 cites W2068606395 @default.
• W2031570299 cites W2069330945 @default.
• W2031570299 cites W2069589985 @default.
• W2031570299 cites W2072046909 @default.
• W2031570299 cites W2072469348 @default.
• W2031570299 cites W2073856024 @default.
• W2031570299 cites W2074655039 @default.
• W2031570299 cites W2077548707 @default.
• W2031570299 cites W2078457332 @default.
• W2031570299 cites W2082657038 @default.
• W2031570299 cites W2082670705 @default.
• W2031570299 cites W2086132387 @default.
• W2031570299 cites W2093873750 @default.
• W2031570299 cites W2094831461 @default.
• W2031570299 cites W2097774235 @default.
• W2031570299 cites W2104788426 @default.
• W2031570299 cites W2116905501 @default.
• W2031570299 cites W2118862408 @default.
• W2031570299 cites W2119368674 @default.
• W2031570299 cites W2126393916 @default.
• W2031570299 cites W2127321901 @default.
• W2031570299 cites W2127632559 @default.
• W2031570299 cites W2129152954 @default.
• W2031570299 cites W2135437310 @default.
• W2031570299 cites W2136235039 @default.
• W2031570299 cites W2136932227 @default.
• W2031570299 cites W2143138913 @default.
• W2031570299 cites W2143358450 @default.
• W2031570299 cites W2145694215 @default.
• W2031570299 cites W2148381523 @default.
• W2031570299 cites W2149517362 @default.
• W2031570299 cites W2150939062 @default.
• W2031570299 cites W2151441544 @default.
• W2031570299 cites W2164670057 @default.
• W2031570299 cites W2166606562 @default.
• W2031570299 cites W2262297515 @default.
• W2031570299 cites W2317775706 @default.
• W2031570299 cites W2318845086 @default.
• W2031570299 cites W2321135911 @default.
• W2031570299 cites W2321753243 @default.
• W2031570299 cites W2328777842 @default.
• W2031570299 cites W2331128316 @default.
• W2031570299 cites W2332136329 @default.
• W2031570299 cites W4231466249 @default.
• W2031570299 cites W9628304 @default.
• W2031570299 doi "https://doi.org/10.1038/sj.onc.1205400" @default.
• W2031570299 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/12032779" @default.
• W2031570299 hasPublicationYear "2002" @default.
• W2031570299 type Work @default.

• next