Deletion of Tet2 in mice leads to dysregulated hematopoietic stem cells and subsequent development of myeloid malignancies.

By Zhe Li, Xiaoqiang Cai, Chengfeng Cai, Jiapeng Wang, Wenyong Zhang, B. Petersen, Feng-Chun Yang, Mingjiang Xu. Blood, 2011

665 citations recorded by the source corpus.

Subfields: Hematology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/4762ebaf5b68893b66e23373f31611a9fab1336f

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In Hematology

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Citations in the corpus

• Reversing DNA Methylation: Mechanisms, Genomics, and Biological Functions (2014, neutral): “Mouse genetic studies have demonstrated that Tet2-deficiency causes enhanced self-renew of hematopoietic stem cells (Ko et al., 2011; Li et al., 2011; Moran-Crusio et al., 2011; Quivoron et al., 2011), supporting a role of TET2 as tumor suppressor for leukemia.”
• Influence of Metabolism on Epigenetics and Disease (2013, positive): “In addition, TET2 inactivation is sufficient to promote hematopoietic stem cell self-renewal and to block differentiation (Figueroa et al., 2010; Li et al., 2011;Moran-Crusio et al., 2011; Noushmehr et al., 2010; Turcan et al., 2012; Losman et al., 2013).”
• Mechanisms and functions of Tet protein-mediated 5-methylcytosine oxidation. (2011, methodology): “The approaches include shRNA-based Tet2 knockdown and targeted deletion of Tet2 in mice (Figueroa et al. 2010; Ko et al. 2010, 2011; Li et al. 2011; MoranCrusio et al. 2011; Quivoron et al. 2011).”
• WT1 recruits TET2 to regulate its target gene expression and suppress leukemia cell proliferation (2015, neutral): “, 2011), differentiation of haematopoietic cells (Ko et al., 2011; Li et al., 2011; Moran-Crusio et al., 2011; Quivoron et al., 2011), and induced pluripotent stem cell (iPSC) reprogramming (Costa et al.”
• Epigenomic profiling of young and aged HSCs reveals concerted changes during aging that reinforce self-renewal (2014, background): “…their functions are unknown, Tet2 mutation leads to expansion of hematopoietic progenitors and increased stem cell self-renewal (Ko et al., 2011; Li et al., 2011; Moran-Crusio et al., 2011; Quivoron et al., 2011), and TET2 is recurrently mutated in myelodysplastic syndrome (MDS) and acute…”
• One-Step Generation of Mice Carrying Mutations in Multiple Genes by CRISPR/Cas-Mediated Genome Engineering (2013, neutral): “Tet proteins (Tet1/2/3) convert 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC) in various embryonic and adult tissues and mutant mice for each of these three genes have been produced by homologous recombination in ES cells (Dawlaty et al., 2011; Gu et al., 2011; Li et al., 2011; Moran-Crus”
• DNA methylation dynamics during epigenetic reprogramming in the germline and preimplantation embryos (2014, background): “Tet1 and Tet2 are detected in ESCs and PGCs. Tet2 expression is essential in hematopoietic cells; knockouts are viable but develop severe, lethal hematopoietic malignancies at 4–6 mo of age (Li et al. 2011; Moran-Crusio et al. 2011; Quivoron et al. 2011; Koh and Rao 2013).”
• Role of TET enzymes in DNA methylation, development, and cancer (2016, background): “Loss of Tet2 results in age-associated extramedullary hematopoiesis and expansion of monocytes and granulocytes in the spleen (Ko et al. 2011; Li et al. 2011; Moran-Crusio et al. 2011; Quivoron et al. 2011; Shide et al. 2012), whereas Tet1 deficiency leads to an overall lymphoid bias and dysregulate”