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Related Concept Videos

Epigenetic Regulation01:37

Epigenetic Regulation

Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
X-chromosome...
Epigenetic Regulation01:46

Epigenetic Regulation

Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
Epigenetic Regulation01:46

Epigenetic Regulation

Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
Covalently Linked Protein Regulators02:04

Covalently Linked Protein Regulators

Proteins can undergo many types of post-translational modifications, often in response to changes in their environment. These modifications play an important role in the function and stability of these proteins. Covalently linked molecules include functional groups, such as methyl, acetyl, and phosphate groups, and also small proteins, such as ubiquitin. There are around 200 different types of covalent regulators that have been identified.
These groups modify specific amino acids in a protein.
Covalently Linked Protein Regulators02:04

Covalently Linked Protein Regulators

Proteins can undergo many types of post-translational modifications, often in response to changes in their environment. These modifications play an important role in the function and stability of these proteins. Covalently linked molecules include functional groups, such as methyl, acetyl, and phosphate groups, and also small proteins, such as ubiquitin. There are around 200 different types of covalent regulators that have been identified.
These groups modify specific amino acids in a protein.
Complementary DNA01:44

Complementary DNA

Overview

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Related Experiment Video

Updated: Jun 3, 2026

Immunoprecipitation with an Anti-Epitope Tag Affinity Gel to Study Protein-Protein Interactions
07:16

Immunoprecipitation with an Anti-Epitope Tag Affinity Gel to Study Protein-Protein Interactions

Published on: January 5, 2024

Epigenetics and complementary proteins.

D Ciavatta1, R J Falk

  • 1UNC Kidney Center, University of North Carolina at Chapel Hill, USA. dominic_ciavatta@med.unc.edu

Clinical and Experimental Immunology
|March 31, 2011
PubMed
Summary
This summary is machine-generated.

Epigenetic silencing defects in neutrophils may drive anti-neutrophil cytoplasm antibody (ANCA) vasculitis by allowing autoantigen gene activation and anti-sense transcript production, potentially leading to complementary protein autoimmunity.

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Area of Science:

  • Immunology
  • Genetics
  • Epigenetics

Background:

  • Research on anti-neutrophil cytoplasm antibody (ANCA) vasculitis traditionally focuses on autoantibodies.
  • Emerging evidence highlights the significance of ANCA autoantigen gene regulation in disease pathogenesis.

Purpose of the Study:

  • To investigate the role of epigenetic regulation and autoantigen gene activity in ANCA vasculitis.
  • To explore the potential involvement of anti-sense transcripts in the disease mechanism.

Main Methods:

  • Transcriptional analysis of neutrophils from ANCA vasculitis patients and healthy controls.
  • Examination of epigenetic silencing mechanisms in neutrophils.

Main Results:

  • ANCA autoantigen genes are transcriptionally active in mature neutrophils of ANCA vasculitis patients, unlike in healthy controls.
  • Neutrophils in ANCA vasculitis exhibit disrupted epigenetic silencing, leading to an unusual transcriptional state.
  • Presence of anti-sense transcripts in ANCA vasculitis patients, potentially linked to complementary protein production.

Conclusions:

  • Failed epigenetic silencing in neutrophils is a key factor in ANCA vasculitis pathogenesis.
  • Anti-sense transcripts may play a pathological role by serving as templates for complementary autoantigen production.
  • Further understanding of epigenetic silencing and complementary proteins could reveal the underlying pathology of ANCA vasculitis.