Target intelligence / Profile preview

Centromere protein S (CENP-S)

Target
CENP-S
Molecular classification
Other (Histone-fold-containing centromere complex protein), DNA-binding protein, Component of Fanconi anemia core complex
01

Overview

Centromere protein S (CENP-S) is a DNA-binding protein that forms part of the constitutive centromere-associated network (CCAN) and is a component of a nucleosome-like complex at the centromere, including CENP-T, CENP-W, and CENP-X[1]. This complex is involved in the structural assembly and functional switching of the centromere during the cell cycle, converting centromeric chromatin into a mitosis-competent state after DNA replication. CENP-S participates in kinetochore assembly by acting as a chromatin receptor for mitotic machinery, and also has a role in the cellular response to DNA damage as a component of the Fanconi anemia (FA) repair pathway, where it is essential for activation of the FA pathway and maintenance of genomic stability[1][3]. Loss or dysfunction of CENP-S can lead to impaired chromosome segregation, genomic instability, and is relevant to cancer and Fanconi anemia pathogenesis. There are currently no drugs that specifically target CENP-S, and it is not employed as a clinical biomarker.

Other names
CENPSFAAP16MHF1APITD1Centromere protein SCENP-SFANCM-associated histone fold protein 1FANCM-interacting histone fold protein 1Fanconi anemia-associated polypeptide of 16 kDaApoptosis-inducing TAF9-like domain-containing protein 1
02

Mechanism of action

No known drugs directly target CENP-S; DNA repair modulation and chromosome segregation are general mechanisms in its pathway

03

Biological functions

Chromatin assembly and structureCentromere and kinetochore formationCell cycle progression (mitosis and S/G2 phase chromatin remodeling)DNA damage response (Fanconi anemia pathway)
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Disease associations

Cancer (due to involvement in chromosome segregation and genomic stability)Fanconi anemiaPotential others relating to defects in DNA repair
05

Safety considerations

Disruption leads to chromosome segregation errors and genomic instabilityDeficient function associated with Fanconi anemia pathway defects

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