Mechanisms that regulate the activities of TET proteins

Joshi, Kanak; Liu, Shanhui; J, Peter Breslin S; Zhang, Jiwang

doi:10.1007/s00018-022-04396-x

Cited by 59 publications

(29 citation statements)

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“…DNA methylation is one of the most typical epigenetic modifications and plays an important role in embryonic development, cell differentiation, genetic imprinting, and regulation of gene expression. , The ten-eleven translocation 1 (TET1) protein is involved in DNA demethylation through iterative oxidation of 5-methylcytosine (5mC) to form 5-hydroxymethylcytosine (5hmC), 5-formylcytosine (5fC), and 5-carboxycytosine (5caC). − It has been found that the TET1 protein is widely present in a variety of cells, which affects the migration, proliferation, and invasion of many types of cancer cells . The levels of TET1 protein usually change significantly with tumorigenesis, and the detection of the changes in its levels can be used to predict disease onset, suggesting that TET1 protein is expected to be a new marker for disease diagnosis and detection. , However, the functional study of the TET1 protein is still unclear, and establishing a facile and selective approach to study the function of TET1 protein is essential.…”

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confidence: 99%

“…6 The levels of TET1 protein usually change significantly with tumorigenesis, and the detection of the changes in its levels can be used to predict disease onset, suggesting that TET1 protein is expected to be a new marker for disease diagnosis and detection. 7,8 However, the functional study of the TET1 protein is still unclear, and establishing a facile and selective approach to study the function of TET1 protein is essential.…”

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confidence: 99%

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MXene Enhanced Photoactivity of Bi₂O₃/Bi₂S₃ Heterojunction with G-wire Superstructure for Photoelectrochemical Detection of TET1 Protein

et al. 2022

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Ten-eleven translocation 1 (TET1) protein has the potential to accelerate the oxygenation of 5-methylcytosine to 5hydroxymethylcytosine (5hmC); then the −CH 2 OH of 5hmC can further covalently react with −SH catalyzed by M.HhaI methyltransferase. A brand-new photoelectrochemical (PEC) detection technique for the TET1 protein was created in light of this. For this objective, the Bi 2 O 3 /Bi 2 S 3 heterojunction was first prepared by a one-pot hydrothermal method and served for photosensitive materials. For further enhancing the photoactivity, Bi 2 O 3 /Bi 2 S 3 was blended with MXene to form an energy bandmatched structure, thus improving the migration kinetics of photogenerated carriers. For achieving a high sensitivity of detection, a DNA Walker incorporated with the nicking endonuclease (Nb.BbvCI enzyme)-assisted signal amplification strategy was presented to output exponential G-quadruplex fragments. Self-assembly of the free G-quadruplex sequence into a G-wire superstructure with the assistance of Mg 2+ provided more loading sites for MB and amplified the PEC signal. The linear range of the biosensor was 0.1−10 μg/mL with a detection limit of 0.024 μg/mL (S/N = 3) for TET1 protein under optimal experimental conditions. The suitability of the proposed method was evaluated by inhibitor screening experiments and the influence of environmental degradation on the activity of TET1 protein.

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confidence: 99%

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confidence: 99%

MXene Enhanced Photoactivity of Bi₂O₃/Bi₂S₃ Heterojunction with G-wire Superstructure for Photoelectrochemical Detection of TET1 Protein

et al. 2022

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“…This suggests that other elements or the structure of Tets may have an influence on the function of the proteins. Indeed, the activities of Tet proteins are regulated by several mechanisms at different levels [ 38 ].…”

Section: Discussionmentioning

confidence: 99%

Early Expression of Tet1 and Tet2 in Mouse Zygotes Altered DNA Methylation Status and Affected Embryonic Development

Wang

Liu

et al. 2022

IJMS

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Ten-eleven translocation (Tet) dioxygenases can induce DNA demethylation by catalyzing 5-methylcytosine(5mC) to 5-hydroxymethylcytosine(5hmC), and play important roles during mammalian development. In mouse, Tet1 and Tet2 are not expressed in pronucleus-staged embryos and are not involved in the genomic demethylation of early zygotes. Here, we investigated the influence of Tet1 and Tet2 on methylation of parental genomes by ectopically expressing Tet1 and Tet2 in zygotes. Immunofluorescence staining showed a marked 5hmC increase in the maternal pronucleus after injection of Tet1 or Tet2 mRNA into zygotes. Whole-genome bisulfite sequencing further revealed that Tet2 greatly enhanced the global demethylation of both parental genomes, while Tet1 only promoted the paternal demethylation. Tet1 and Tet2 overexpression altered the DNA methylation across genomes, including various genic elements and germline-specific differently methylated regions. Tet2 exhibited overall stronger demethylation activity than Tet1. Either Tet1 or Tet2 overexpression impaired preimplantation embryonic development. These results demonstrated that early expression of Tet1 and Tet2 could substantially alter the zygotic methylation landscape and damage embryonic development. These findings provide new insights into understanding the function of Tet dioxygenases and the mechanism of DNA methylation in relation to embryogenesis.

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“…The ten-eleven translocation (TET) family of dioxygenases consists of TET1, TET2, and TET3. All three TET proteins catalyze the dynamic DNA demethylation process by converting 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC), and further oxidizing 5hmC to 5-formylcytosine and 5-carboxylcytosine [3,4]. TET proteins also regulate histone modifications including H3K4 methylation, H3K27 acetylation, and H2B monoubiquitylation by recruiting Set1/COM-PASS and PRC1/2 complexes, all independent of their enzymatic activities [4][5][6].…”

Section: Introductionmentioning

confidence: 99%

“…All three TET proteins catalyze the dynamic DNA demethylation process by converting 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC), and further oxidizing 5hmC to 5-formylcytosine and 5-carboxylcytosine [3,4]. TET proteins also regulate histone modifications including H3K4 methylation, H3K27 acetylation, and H2B monoubiquitylation by recruiting Set1/COM-PASS and PRC1/2 complexes, all independent of their enzymatic activities [4][5][6]. TET proteins play such roles by collaborating with lineage-specific transcription factors (TFs), which determine the site-specific reconfiguration of the epigenetic landscape [7][8][9].…”

Section: Introductionmentioning

confidence: 99%

Role of TET dioxygenases in the regulation of both normal and pathological hematopoiesis

Joshi

Zhang²,

S.J.³

et al. 2022

J Exp Clin Cancer Res

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The family of ten-eleven translocation dioxygenases (TETs) consists of TET1, TET2, and TET3. Although all TETs are expressed in hematopoietic tissues, only TET2 is commonly found to be mutated in age-related clonal hematopoiesis and hematopoietic malignancies. TET2 mutation causes abnormal epigenetic landscape changes and results in multiple stages of lineage commitment/differentiation defects as well as genetic instability in hematopoietic stem/progenitor cells (HSPCs). TET2 mutations are founder mutations (first hits) in approximately 40–50% of cases of TET2-mutant (TET2MT) hematopoietic malignancies and are later hits in the remaining cases. In both situations, TET2MT collaborates with co-occurring mutations to promote malignant transformation. In TET2MT tumor cells, TET1 and TET3 partially compensate for TET2 activity and contribute to the pathogenesis of TET2MT hematopoietic malignancies. Here we summarize the most recent research on TETs in regulating of both normal and pathogenic hematopoiesis. We review the concomitant mutations and aberrant signals in TET2MT malignancies. We also discuss the molecular mechanisms by which concomitant mutations and aberrant signals determine lineage commitment in HSPCs and the identity of hematopoietic malignancies. Finally, we discuss potential strategies to treat TET2MT hematopoietic malignancies, including reverting the methylation state of TET2 target genes and targeting the concomitant mutations and aberrant signals.

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Mechanisms that regulate the activities of TET proteins

Cited by 59 publications

References 306 publications

MXene Enhanced Photoactivity of Bi₂O₃/Bi₂S₃ Heterojunction with G-wire Superstructure for Photoelectrochemical Detection of TET1 Protein

MXene Enhanced Photoactivity of Bi₂O₃/Bi₂S₃ Heterojunction with G-wire Superstructure for Photoelectrochemical Detection of TET1 Protein

Early Expression of Tet1 and Tet2 in Mouse Zygotes Altered DNA Methylation Status and Affected Embryonic Development

Role of TET dioxygenases in the regulation of both normal and pathological hematopoiesis

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Mechanisms that regulate the activities of TET proteins

Cited by 59 publications

References 306 publications

MXene Enhanced Photoactivity of Bi2O3/Bi2S3 Heterojunction with G-wire Superstructure for Photoelectrochemical Detection of TET1 Protein

MXene Enhanced Photoactivity of Bi2O3/Bi2S3 Heterojunction with G-wire Superstructure for Photoelectrochemical Detection of TET1 Protein

Early Expression of Tet1 and Tet2 in Mouse Zygotes Altered DNA Methylation Status and Affected Embryonic Development

Role of TET dioxygenases in the regulation of both normal and pathological hematopoiesis

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MXene Enhanced Photoactivity of Bi₂O₃/Bi₂S₃ Heterojunction with G-wire Superstructure for Photoelectrochemical Detection of TET1 Protein

MXene Enhanced Photoactivity of Bi₂O₃/Bi₂S₃ Heterojunction with G-wire Superstructure for Photoelectrochemical Detection of TET1 Protein