NCAPH

NCAPH
Identifiers
Aliases	NCAPH, BRRN1, CAP-H, non-SMC condensin I complex subunit H
External IDs	MGI: 2444777 HomoloGene: 133986 GeneCards: NCAPH
Gene ontology Molecular function • protein binding Cellular component • cytoplasm • cytosol • membrane • nucleus • chromosome • condensin complex Biological process • cell division • cell cycle • mitotic nuclear division • chromosome condensation • mitotic chromosome condensation Sources:Amigo / QuickGO
RNA expression pattern
More reference expression data
Orthologs
Species	Human	Mouse
Entrez	23397	215387
Ensembl	ENSG00000121152	ENSMUSG00000034906
UniProt	Q15003	Q8C156
RefSeq (mRNA)	NM_001281710 NM_001281711 NM_001281712 NM_015341	NM_144818
RefSeq (protein)	NP_001268639.1 NP_001268640.1 NP_001268641.1 NP_056156.2	NP_659067.2
Location (UCSC)	Chr 2: 96.34 – 96.37 Mb	Chr 2: 127.1 – 127.13 Mb
PubMed search	[1]	[2]
Wikidata

Condensin complex subunit 2 also known as chromosome-associated protein H (CAP-H) or non-SMC condensin I complex subunit H (NCAPH) is a protein that in humans is encoded by the NCAPH gene.^[3][4] CAP-H is a subunit of condensin I, a large protein complex involved in chromosome condensation

Function

CAP-H is a member of the barr protein family and a regulatory subunit of the condensin complex. This complex is required for the conversion of interphase chromatin into condensed chromosomes. CAP-H is associated with mitotic chromosomes, except during the early phase of chromosome condensation. During interphase, the protein has a distinct punctate nucleolar localization.^[4]

Model organisms

Model organisms have been used in the study of NCAPH function. A conditional knockout mouse line, called Ncaph^{tm1a(EUCOMM)Wtsi[9][10]} was generated as part of the International Knockout Mouse Consortium program — a high-throughput mutagenesis project to generate and distribute animal models of disease to interested scientists.^[11][12][13]

Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion.^[7][14] Twenty four tests were carried out on mutant mice and three significant abnormalities were observed.^[7] No homozygous mutant embryos were identified during gestation, and therefore none survived until weaning. The remaining tests were carried out on heterozygous mutant adult mice and an increased susceptibility to bacterial infection was observed in male animals.^[7]

References

Further reading