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Related Concept Videos

Circadian Rhythms and Gene Regulation02:19

Circadian Rhythms and Gene Regulation

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The biological clock is involved in many aspects of regulating complex physiology in all animals. It was in 1935 when German zoologists, Hans Kalmus and Erwin Bünning, discovered the existence of circadian rhythm in Drosophila melanogaster. However, the internal molecular mechanisms behind the circadian clock remained a mystery until 1984, when Jeffrey C. Hall, Michael Rosbash, and Michael W. Young discovered the expression of the Per gene oscillating over a 24-hour cycle. In subsequent...
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Circadian rhythms are cyclic changes that are crucial in plasma drug concentrations. Various standard circadian parameters, including core body temperature, heart rate, and other cardiovascular factors, directly impact disease states and the therapeutic response to drug therapy.
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Genetic Variation01:25

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Genetic variation is the diversity in DNA sequences found among individuals of the same species. This diversity is crucial for a species' survival because it helps organisms adapt to environmental changes. Genetic variation begins with fertilization, where an egg and sperm cell merge. Each of these cells carries 23 chromosomes, up to 46 in the fertilized egg. Chromosomes are long DNA strands that contain genes, the basic units of heredity.
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Histone variants are the histone proteins with structural and sequence variations. These variants may be regarded as “mutant” forms that replace their canonical histone counterparts in the nucleosomes. Specific post-translational modifications on the histone variants enable further chromatin complexity and regulate tissue-specific gene expression. The most common histone variants are from histone H2A, H2B, and linker histone H1 families. However, several variants of histone H3...
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Related Experiment Video

Updated: Apr 14, 2026

Parallel Measurement of Circadian Clock Gene Expression and Hormone Secretion in Human Primary Cell Cultures
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Genetic variability within molecular core clock genes in cluster headache.

Clémence Deborgies Sanches1, Stefan Spulber1, Felicia Jennysdotter Olofsgård1

  • 1Centre for Cluster Headache, Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden.

Cephalalgia : an International Journal of Headache
|April 12, 2026
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Summary

Cluster headache attacks show circadian rhythmicity, suggesting molecular clock dysfunction. Genetic markers in core clock genes, particularly BMAL1 and NPAS2, were associated with increased cluster headache risk, implicating clock gene variations in the condition.

Keywords:
ARNTL1BMAL1NPAS2circadiansleep

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Area of Science:

  • Genetics
  • Chronobiology
  • Neurology

Background:

  • Cluster headache attacks exhibit circadian rhythmicity in a majority of patients.
  • This suggests potential dysregulation of the molecular clock mechanism.

Purpose of the Study:

  • To investigate the association between genetic markers in core clock genes and the genetic risk for cluster headache.
  • To explore the combined effects of these genetic markers on cluster headache susceptibility.

Main Methods:

  • Genotyping of seven markers in BMAL1 and NPAS2 using TaqMan qPCR in 707 cluster headache patients and 682 controls.
  • Analysis of genetic data from eleven additional markers in CLOCK, CRY1-2, and PER1-3.
  • Risk analysis for combinations of up to three markers, with validation in a UK cohort.

Main Results:

  • Single marker analysis identified rs3789327 and rs3768984 in BMAL1 and NPAS2 as more frequent in cluster headache patients.
  • Combinatorial analysis revealed 258 significant risk-associated combinations of up to three markers.
  • Eighty percent of these combinations involved markers in the positive arm of the molecular clock transcription-translation feedback loop (TTFL).
  • Replication in a UK cohort confirmed risk associated with rs3768984 and enrichment of BMAL1, CLOCK, and NPAS2 markers.

Conclusions:

  • Genetic variations in core clock genes contribute to the genetic risk of cluster headache.
  • Molecular clock dysfunction is implicated as a central factor in cluster headache pathogenesis.
  • Specific combinations of clock gene markers may enhance cluster headache susceptibility.