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Inheritance of Chromatin Structures03:17

Inheritance of Chromatin Structures

Epigenetics is the study of inherited changes in a cell's phenotype without changing the DNA sequences. It provides a form of memory for the differential gene expression pattern to maintain cell lineage, position-effect variegation, dosage compensation, and maintenance of chromatin structures such as telomeres and centromeres. For example, the structure and location of the centromere on chromosomes are epigenetically inherited. Its functionality is not dictated or ensured by the underlying DNA...
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The human X chromosome contains over ten times the number of genes as in the Y chromosome. Since males have only one X chromosome, and females have two, one might expect females to produce twice as many of the proteins, with undesirable results.
X-inactivation01:58

X-inactivation

The human X chromosome contains over ten times the number of genes as in the Y chromosome. Since males have only one X chromosome, and females have two, one might expect females to produce twice as many of the proteins, with undesirable results.
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Exon Recombination

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Ligand-gated Ion Channels01:19

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Ligand-gated ion channels fall into three subfamilies. The 'Cys-loop' includes the nicotinic acetylcholine receptors, γ-aminobutyric acid (GABA), glycine, and 5-hydroxytryptamine receptors. The second one is the 'Pore-loop' channels that include the...
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Updated: May 8, 2026

A Non-random Mouse Model for Pharmacological Reactivation of Mecp2 on the Inactive X Chromosome
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Published on: May 22, 2019

XIST Is a Key Modulator Associated with the Adhesome Network.

Dongning Chen, Nolan Origer, Sha Sun

    Biorxiv : the Preprint Server for Biology
    |May 7, 2026
    PubMed
    Summary
    This summary is machine-generated.

    The X-inactivation specific transcript (XIST) long non-coding RNA regulates cell adhesion and stemness. XIST modulates the adhesome network, impacting cancer cell plasticity and clinical outcomes.

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    11:13

    Stem cell-like Xenopus Embryonic Explants to Study Early Neural Developmental Features In Vitro and In Vivo

    Published on: February 2, 2016

    Area of Science:

    • Epigenetics
    • Cancer Biology
    • Molecular Biology

    Background:

    • The X-inactivation specific transcript (XIST) long non-coding RNA is crucial for X chromosome inactivation and dosage compensation.
    • While XIST's role in development is established, emerging evidence suggests non-canonical functions in cancer stemness and cellular plasticity.
    • The adhesome network, comprising cell adhesion molecules, is integral to regulating cancer stemness.

    Purpose of the Study:

    • To investigate the previously unrecognized link between XIST and the adhesome network.
    • To explore XIST's role in regulating cell adhesion pathways and its association with cancer stemness.

    Main Methods:

    • Gene expression and gene ontology analysis were performed on XIST-knockdown ovarian cancer cells.
    • Genotype-Tissue Expression (GTEx) and The Cancer Genome Atlas (TCGA) datasets were utilized to analyze XIST and adhesome gene correlations.
    • Network analysis and hazard ratio analysis were employed to assess interactions and clinical implications.

    Main Results:

    • XIST knockdown significantly altered adhesome gene expression and downstream adhesion pathways in ovarian cancer cells.
    • Distinct correlations between XIST lncRNA and adhesome genes were identified across normal and cancer tissues, associated with cell stemness.
    • Network analysis suggested potential nuclear interactions between XIST and specific adhesome genes, with functional implications for clinical outcomes.

    Conclusions:

    • XIST acts as a modulator strongly associated with the adhesome network and cell stemness.
    • A novel link between lncRNA-mediated epigenetic regulation of cell adhesion genes and cancer stemness is supported.
    • XIST is highlighted as a key regulator contributing to the adhesome network, with potential implications for cancer development and progression.