FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2065160134> ?p ?o ?g. }

• W2065160134 endingPage "1099" @default.
• W2065160134 startingPage "1093" @default.
• W2065160134 abstract "DNA methylation is one of the critical epigenetic modifications regulating various cellular processes such as differentiation or proliferation, and its dysregulation leads to disordered stem cell function or cellular transformation. The ten-eleven translocation (TET) gene family, initially found as a chromosomal translocation partner in leukemia, turned out to be a key enzyme for DNA demethylation. TET genes hydroxylate 5-methylcytosine to 5-hydroxymethylcytosine, which is then converted to unmodified cytosine through multiple mechanisms. Somatic mutations of the TET2 gene were reported in a variety of human hematological malignancies such as leukemia, myelodysplastic syndrome, and malignant lymphoma, suggesting a critical role for TET2 in hematopoiesis. The importance of the TET-mediated cytosine demethylation pathway is also underscored by a recurrent mutation of isocitrate dehydrogenase 1 (IDH1) and IDH2 in hematological malignancies, whose mutation inhibits TET function through a novel oncometabolite, 2-hydroxyglutarate. Studies using mouse models revealed that TET2 is critical for the function of hematopoietic stem cells, and disruption of TET2 results in the expansion of multipotent as well as myeloid progenitors, leading to the accumulation of premalignant clones. In addition to cytosine demethylation, TET proteins are involved in chromatin modifications and other cellular processes through the interaction with O-linked β-N-acetylglucosamine transferase. In summary, TET2 is a critical regulator for hematopoietic stem cell homeostasis whose functional impairment leads to hematological malignancies. Future studies will uncover the whole picture of epigenetic and signaling networks wired with TET2, which will help to develop ways to intervene in cellular pathways dysregulated by TET2 mutations." @default.
• W2065160134 created "2016-06-24" @default.
• W2065160134 creator A5036193214 @default.
• W2065160134 creator A5052090382 @default.
• W2065160134 date "2014-09-01" @default.
• W2065160134 modified "2023-10-01" @default.
• W2065160134 title "<scp> <i>TET2</i> </scp> as an epigenetic master regulator for normal and malignant hematopoiesis" @default.
• W2065160134 cites W1255676896 @default.
• W2065160134 cites W1914113311 @default.
• W2065160134 cites W1964487182 @default.
• W2065160134 cites W1969013165 @default.
• W2065160134 cites W1978867062 @default.
• W2065160134 cites W1991219645 @default.
• W2065160134 cites W1993236149 @default.
• W2065160134 cites W1993627126 @default.
• W2065160134 cites W1995675594 @default.
• W2065160134 cites W1997308620 @default.
• W2065160134 cites W1997453048 @default.
• W2065160134 cites W1997556856 @default.
• W2065160134 cites W1997998180 @default.
• W2065160134 cites W1998367819 @default.
• W2065160134 cites W2002582477 @default.
• W2065160134 cites W2003217864 @default.
• W2065160134 cites W2005351392 @default.
• W2065160134 cites W2009447162 @default.
• W2065160134 cites W2012701284 @default.
• W2065160134 cites W2026134786 @default.
• W2065160134 cites W2027343725 @default.
• W2065160134 cites W2028078153 @default.
• W2065160134 cites W2029050314 @default.
• W2065160134 cites W2035166160 @default.
• W2065160134 cites W2036662877 @default.
• W2065160134 cites W2036848594 @default.
• W2065160134 cites W2038449573 @default.
• W2065160134 cites W2040827479 @default.
• W2065160134 cites W2041598067 @default.
• W2065160134 cites W2041686632 @default.
• W2065160134 cites W2046387526 @default.
• W2065160134 cites W2046623240 @default.
• W2065160134 cites W2053930062 @default.
• W2065160134 cites W2066998182 @default.
• W2065160134 cites W2067797084 @default.
• W2065160134 cites W2071445941 @default.
• W2065160134 cites W2071520055 @default.
• W2065160134 cites W2072713007 @default.
• W2065160134 cites W2073415397 @default.
• W2065160134 cites W2073872690 @default.
• W2065160134 cites W2074678620 @default.
• W2065160134 cites W2074822409 @default.
• W2065160134 cites W2078972833 @default.
• W2065160134 cites W2080452140 @default.
• W2065160134 cites W2085293170 @default.
• W2065160134 cites W2093664191 @default.
• W2065160134 cites W2094247278 @default.
• W2065160134 cites W2094703195 @default.
• W2065160134 cites W2095293920 @default.
• W2065160134 cites W2097743943 @default.
• W2065160134 cites W2107279676 @default.
• W2065160134 cites W2108664872 @default.
• W2065160134 cites W2112590089 @default.
• W2065160134 cites W2116205277 @default.
• W2065160134 cites W2126817554 @default.
• W2065160134 cites W2127738065 @default.
• W2065160134 cites W2129270269 @default.
• W2065160134 cites W2129614320 @default.
• W2065160134 cites W2131860315 @default.
• W2065160134 cites W2134061682 @default.
• W2065160134 cites W2146146853 @default.
• W2065160134 cites W2152807349 @default.
• W2065160134 cites W2154677603 @default.
• W2065160134 cites W2157458089 @default.
• W2065160134 cites W2159731673 @default.
• W2065160134 cites W2169172058 @default.
• W2065160134 cites W2487821414 @default.
• W2065160134 cites W4233431843 @default.
• W2065160134 doi "https://doi.org/10.1111/cas.12484" @default.
• W2065160134 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4462392" @default.
• W2065160134 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25040794" @default.
• W2065160134 hasPublicationYear "2014" @default.
• W2065160134 type Work @default.
• W2065160134 sameAs 2065160134 @default.
• W2065160134 citedByCount "87" @default.
• W2065160134 countsByYear W20651601342015 @default.
• W2065160134 countsByYear W20651601342016 @default.
• W2065160134 countsByYear W20651601342017 @default.
• W2065160134 countsByYear W20651601342018 @default.
• W2065160134 countsByYear W20651601342019 @default.
• W2065160134 countsByYear W20651601342020 @default.
• W2065160134 countsByYear W20651601342021 @default.
• W2065160134 countsByYear W20651601342022 @default.
• W2065160134 countsByYear W20651601342023 @default.
• W2065160134 crossrefType "journal-article" @default.
• W2065160134 hasAuthorship W2065160134A5036193214 @default.
• W2065160134 hasAuthorship W2065160134A5052090382 @default.
• W2065160134 hasBestOaLocation W20651601341 @default.
• W2065160134 hasConcept C104317684 @default.
• W2065160134 hasConcept C109159458 @default.
• W2065160134 hasConcept C150194340 @default.

• next