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Related Concept Videos

The Y Chromosome Determines Maleness02:19

The Y Chromosome Determines Maleness

The Y chromosome is a sex chromosome found in several vertebrates and mammals, including humans. In addition to 22 pairs of autosomes, the human males have one X chromosome and one Y chromosome. In these organisms, the presence or absence of the Y chromosome determines the development of male traits.
Evolution
Around 300 million years ago, the two sex chromosomes diverged from two identical autosomal chromosomes. Over time, the Y chromosome has lost most of its genes, shrinking in size. Today,...
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Specialized Characteristics of Cardiac Muscles

The primary role of cardiac muscles is to propel blood throughout the cardiovascular system. The cardiac muscle cells, or cardiomyocytes, exhibit specialized characteristics that allow them to perform this function.
Cardiac muscle cells are smaller than skeletal muscles, averaging 10–20 mm in diameter and 50–100 mm in length. However, they have large energy demands for continuous contraction and relaxation. This energy is almost exclusively derived from aerobic metabolism of energy reserves in...

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Updated: May 21, 2026

A Reverse Genetic Approach to Test Functional Redundancy During Embryogenesis
06:59

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Published on: August 11, 2010

Myocardial YBX1 is dispensable for cardiac development and function.

Elise V Stanley1, Zhijie Han1, Reaghan Sassower1

  • 1Department of Biomedical Research and Translational Medicine, Masonic Medical Research Institute, Utica, New York, United States.

American Journal of Physiology. Heart and Circulatory Physiology
|May 19, 2026
PubMed
Summary

Yeast-binding protein X1 (YBX1) is crucial for cellular functions. Cardiomyocyte-specific YBX1 deletion in mice did not cause heart defects, suggesting a safe therapeutic target. However, YBX1 loss in other heart cells may be detrimental.

Keywords:
YBX1gene regulationheart developmentheart diseasemouse model

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Published on: November 3, 2011

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Last Updated: May 21, 2026

A Reverse Genetic Approach to Test Functional Redundancy During Embryogenesis
06:59

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Published on: August 11, 2010

Efficient Derivation of Human Cardiac Precursors and Cardiomyocytes from Pluripotent Human Embryonic Stem Cells with Small Molecule Induction
10:46

Efficient Derivation of Human Cardiac Precursors and Cardiomyocytes from Pluripotent Human Embryonic Stem Cells with Small Molecule Induction

Published on: November 3, 2011

Area of Science:

  • Molecular Biology
  • Cardiovascular Biology
  • Genetics

Background:

  • Yeast-binding protein X1 (YBX1) is a DNA/RNA-binding protein regulating gene expression and cellular functions.
  • YBX1 dysregulation is implicated in heart disease, but its precise role in the heart is unclear due to conflicting findings from previous studies.
  • Existing loss-of-function studies using RNA interference (RNAi) are limited by off-target effects and lack of cell specificity.

Purpose of the Study:

  • To investigate the specific role of YBX1 in cardiomyocytes and its impact on cardiac function and development.
  • To create and analyze cardiac-specific YBX1 knockout mouse models to overcome limitations of previous studies.
  • To determine the safety of targeting YBX1 therapeutically in the context of heart disease.

Main Methods:

  • Construction of global and cardiomyocyte-specific Ybx1 knockout (KO) mouse models.
  • Phenotypic analysis of global Ybx1 KO mice, including assessment of embryonic lethality and cardiac development.
  • Detailed evaluation of cardiomyocyte-specific Ybx1 KO (Ybx1cmKO) mice for cardiac morphology, function, and gene expression changes using RNA-sequencing.

Main Results:

  • Global Ybx1 KO mice exhibited embryonic lethality with severe cardiac defects, including noncompaction and impaired septal development.
  • Ybx1cmKO mice showed no apparent morphological abnormalities or cardiac dysfunction, indicating YBX1 is dispensable in cardiomyocytes for heart development and function.
  • RNA-sequencing in Ybx1cmKO hearts revealed upregulation of some fibrosis-related genes, but without resulting in cardiac fibrosis.

Conclusions:

  • YBX1 is essential for embryonic development, with global loss leading to lethal cardiac defects.
  • Specific deletion of YBX1 in cardiomyocytes does not induce cardiac hypertrophy, fibrosis, or dysfunction.
  • Targeting YBX1 specifically within cardiomyocytes may be a safe therapeutic strategy for heart disease, but YBX1's role in other cardiac cell types requires careful consideration.