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Related Concept Videos

Mismatch Repair01:20

Mismatch Repair

Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...
Mismatch Repair01:36

Mismatch Repair

Overview
Translation01:31

Translation

Lesson: Translation
Translation is the process of synthesizing proteins from the genetic information carried by messenger RNA (mRNA). Following transcription, it constitutes the final step in the expression of genes. This process is carried out by ribosomes, complexes of protein and specialized RNA molecules. Ribosomes, transfer RNA (tRNA), and other proteins produce a chain of amino acids—the polypeptide—as the end product of translation.
Translation Produces the Building Blocks of Life
Translation01:31

Translation

Lesson: Translation
Translation is the process of synthesizing proteins from the genetic information carried by messenger RNA (mRNA). Following transcription, it constitutes the final step in the expression of genes. This process is carried out by ribosomes, complexes of protein and specialized RNA molecules. Ribosomes, transfer RNA (tRNA), and other proteins produce a chain of amino acids—the polypeptide—as the end product of translation.
Translation Produces the Building Blocks of Life
Mutations01:39

Mutations

Overview
Mutations01:35

Mutations

Mutations are changes in the sequence of DNA. These changes can occur spontaneously or they can be induced by exposure to environmental factors. Mutations can be characterized in a number of different ways: whether and how they alter the amino acid sequence of the protein, whether they occur over a small or large area of DNA, and whether they occur in somatic cells or germline cells.
Chromosomal Alterations Are Large-Scale Mutations
While point mutations are changes in a single nucleotide in...

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In Vivo Functional Study of Disease-associated Rare Human Variants Using Drosophila
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Published on: August 20, 2019

TET2-CHIP: From Mutation to Malady.

Heng Jian1,2,3,4, Mingyang Sun1,2,3,4, Xinyi Xia1,2,3,4

  • 1Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|May 26, 2026
PubMed
Summary
This summary is machine-generated.

Clonal hematopoiesis (CHIP) with TET2 mutations is linked to cardiovascular disease (CVD) and inflammation. This review explores TET2 biology, CHIP development, and its impact on cardiovascular health.

Keywords:
TET2cardiovascular diseaseclonal hematopoiesis

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Area of Science:

  • Hematology
  • Genetics
  • Cardiovascular Medicine

Background:

  • Clonal hematopoiesis of intermediate potential (CHIP) involves somatic mutations in hematopoietic cells without overt malignancy.
  • TET2 mutations are prevalent in CHIP and strongly associated with cardiovascular disease (CVD) and chronic inflammation.
  • TET2 gene encodes a methylcytosine dioxygenase crucial for epigenetic regulation, and its loss affects hematopoietic stem cell differentiation and mature cell function.

Purpose of the Study:

  • To review the current understanding of TET2 biology.
  • To summarize mechanisms of TET2-CHIP development.
  • To discuss the cardiovascular implications of TET2-CHIP.

Main Methods:

  • Literature review of studies on TET2 biology, CHIP, and cardiovascular disease.
  • Synthesis of evidence linking TET2 mutations to CVD incidence and prognosis.
  • Exploration of potential therapeutic strategies for TET2-CHIP-associated CVD.

Main Results:

  • TET2 loss impairs hematopoietic stem cell differentiation and alters myeloid and lymphoid cell functions.
  • Factors like aging, inflammation, lifestyle, metabolic disorders, cancer therapy, and HIV infection influence TET2-mutant clone emergence and expansion.
  • Growing evidence links TET2-CHIP to the incidence and prognosis of various cardiovascular diseases.

Conclusions:

  • TET2-CHIP is increasingly recognized for its significant role in cardiovascular disease.
  • Understanding TET2 biology and CHIP mechanisms is crucial for addressing associated cardiovascular risks.
  • Emerging therapeutic strategies show promise for managing TET2-CHIP-related cardiovascular complications.