Cenp-a
Cenp-a - Related Videos
09:02
Mass Spectrometry Analysis to Identify Ubiquitylation of EYFP-tagged CENP-A (EYFP-CENP-A)
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Cited by 2 •
2020
CENP-A ubiquitylation is an important requirement for CENP-A deposition at the centromere, inherited through dimerization between cell division, and indispensable to cell viability. Here we describe mass spectrometry analysis to identify ubiquitylation of EYFP-tagged CENP-A (EYFP-CENP-A) protein.
11:49
Generation of Centromere-Associated Protein-E CENP-E-/- Knockout Cell Lines using the CRISPR/Cas9 System
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2023
This article reports the construction of centromere-associated protein-E (CENP-E) knockout cells using the CRISPR/Cas9 system and three phenotype-based screening strategies. We have utilized the CENP-E knockout cell line to establish a novel approach to validate the specificity and toxicity of the CENP-E inhibitors, which is useful for drug development and biological research.
09:41
Functional Assessment of Kinesin-7 CENP-E in Spermatocytes Using In Vivo Inhibition, Immunofluorescence and Flow Cytometry
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Cited by 1 •
2021
This article reports an in vivo inhibition of CENP-E through abdominal surgery and testicular injection of GSK923295, a valuable model for male meiotic division. Using the immunofluorescence, flow cytometry and transmission electron microscopy assays, we show that CENP-E inhibition results in chromosome misalignment and genome instability in mouse spermatocytes.
02:30
Histone Variants at the Centromere
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2020
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 variants are also...
05:35
Immunofluorescence Analysis of Endogenous and Exogenous Centromere-kinetochore Proteins
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Cited by 4 •
2016
Here we report protocols to detect endogenous and exogenous centromere-kinetochore proteins in human cells and quantify these protein levels at centromeres-kinetochores by indirect immunofluorescent staining through the use of fixation (paraformaldehyde, acetone, or methanol fixation).
FAQs
CENP-A deposition and inheritance preserve centromere identity across replication. Controlled placement ensures that newly replicated chromosomes retain a recognizable centromeric platform rather than losing positional information during genome duplication. This continuity allows centromere proteins to assemble appropriately in later cell-cycle stages, supporting kinetochore formation and the chromosome–spindle connection required for accurate segregation.
The CENP-A-containing platform provides the centromere with the molecular basis for recruiting additional centromere proteins. Their assembly creates the kinetochore, the structure that connects each chromosome to spindle microtubules. This organization converts centromere identity into a functional chromosome-segregation interface, linking epigenetic information at the chromosome to the mechanical events of cell division.
Disrupted CENP-A localization or abundance can impair kinetochore function. Because the centromere depends on an appropriately maintained CENP-A platform, such errors can interfere with chromosome attachment to spindle microtubules and increase the risk of chromosome-segregation defects. The resulting chromosomal imbalance provides a direct connection between faulty centromere regulation and compromised genome stability.
A useful investigation considers CENP-A localization, abundance, deposition, and inheritance together with kinetochore function and chromosome segregation. Examining these linked features helps distinguish a problem in centromere maintenance from a later defect in kinetochore activity. This framework can reveal how changes in a centromeric epigenetic platform influence chromosome behavior during cell division.
CENP-A research clarifies how cells preserve centromere identity while chromosomes are replicated and segregated. By connecting deposition and inheritance with kinetochore performance, studies can identify points at which chromosome partitioning becomes unreliable. These findings contribute to a broader understanding of the cellular mechanisms that maintain genome stability and prevent chromosomal imbalance.
Errors affecting CENP-A can disrupt centromere organization, kinetochore function, and chromosome segregation, processes essential for distributing genetic material accurately during cell division. Studying these failures helps connect altered chromosome behavior with developmental abnormalities and disease mechanisms. CENP-A therefore serves as a useful focus for examining how cellular responses to chromosomal imbalance arise.