SUPT7L

SUPT7L
Identifiers
Aliases	SUPT7L, SPT7L, STAF65, STAF65(gamma), STAF65G, SUPT7H, SPT7-like STAGA complex gamma subunit, SPT7 like, STAGA complex gamma subunit, SPT7 like, STAGA complex subunit gamma
External IDs	OMIM: 612762 MGI: 1919445 HomoloGene: 8907 GeneCards: SUPT7L
Gene location (Human)
Chr.	Chromosome 2 (human)[1]
End	27,663,840 bp[1]
Gene location (Mouse)
Chr.	Chromosome 5 (mouse)[2]
End	31,527,807 bp[2]
RNA expression pattern
	; ; ; ;
	More reference expression data
Gene ontology
Molecular function	• GO:0001105 transcription coactivator activity; • GO:0001948 protein binding; • histone acetyltransferase activity; • protein heterodimerization activity;
Cellular component	• STAGA complex; • cell nucleus; • nucleoplasm;
Biological process	• regulation of transcription, DNA-templated; • maintenance of protein location in nucleus; • histone H3 acetylation; • transcription, DNA-templated; • positive regulation of nucleic acid-templated transcription;
	Sources:Amigo / QuickGO
Orthologs
	9913
	72195
	ENSG00000119760
	ENSMUSG00000053134
	O94864
	Q9CZV5
	NM_001282729; NM_001282730; NM_001282731; NM_001282732; NM_014860
	NM_028150
	NP_001269658; NP_001269659; NP_001269660; NP_001269661; NP_055675
	NP_082426
	Wikidata
View/Edit Human	View/Edit Mouse

STAGA complex 65 subunit gamma is a protein that in humans is encoded by the SUPT7L gene.[5][6][7]

Model organisms

*Supt7l* knockout mouse phenotype
Characteristic	Phenotype
Homozygote viability	Abnormal
Recessive lethal study	Abnormal
Fertility	Normal
Body weight	Normal
Anxiety	Normal
Neurological assessment	Normal
Grip strength	Normal
Hot plate	Normal
Dysmorphology	Normal[8]
Indirect calorimetry	Normal
Glucose tolerance test	Normal
Auditory brainstem response	Normal
DEXA	Normal
Radiography	Normal
Body temperature	Normal
Eye morphology	Normal
Clinical chemistry	Normal
Haematology	Normal
Peripheral blood lymphocytes	Normal
Micronucleus test	Normal
Heart weight	Normal
Eye Histopathology	Normal
Salmonella infection	Normal[9]
Citrobacter infection	Normal[10]
All tests and analysis from[11][12]

Model organisms have been used in the study of SUPT7L function. A conditional knockout mouse line, called Supt7l^{tm1a(EUCOMM)Wtsi}[13][14] 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.[15][16][17]

Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion.[11][18] Twenty four tests were carried out on mutant mice and two significant abnormalities were observed.[11] 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 but no further abnormalities were observed.[11]

Interactions

SUPT7L has been shown to interact with TAF9[6] and Transcription initiation protein SPT3 homolog.[6]

References

GRCh38: Ensembl release 89: ENSG00000119760 - Ensembl, May 2017
GRCm38: Ensembl release 89: ENSMUSG00000053134 - Ensembl, May 2017
"Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
"Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
Nagase T, Ishikawa K, Suyama M, Kikuno R, Miyajima N, Tanaka A, Kotani H, Nomura N, Ohara O (October 1998). "Prediction of the coding sequences of unidentified human genes. XI. The complete sequences of 100 new cDNA clones from brain which code for large proteins in vitro". DNA Research. 5 (5): 277–86. doi:10.1093/dnares/5.5.277. PMID 9872452.
Martinez E, Palhan VB, Tjernberg A, Lymar ES, Gamper AM, Kundu TK, Chait BT, Roeder RG (October 2001). "Human STAGA complex is a chromatin-acetylating transcription coactivator that interacts with pre-mRNA splicing and DNA damage-binding factors in vivo". Molecular and Cellular Biology. 21 (20): 6782–95. doi:10.1128/MCB.21.20.6782-6795.2001. PMC 99856. PMID 11564863.
"Entrez Gene: SUPT7L suppressor of Ty 7 (S. cerevisiae)-like".
"Dysmorphology data for Supt7l". Wellcome Trust Sanger Institute.
"Salmonella infection data for Supt7l". Wellcome Trust Sanger Institute.
"Citrobacter infection data for Supt7l". Wellcome Trust Sanger Institute.
Gerdin AK (2010). "The Sanger Mouse Genetics Programme: High throughput characterisation of knockout mice". Acta Ophthalmologica. 88: 925–7. doi:10.1111/j.1755-3768.2010.4142.x. S2CID 85911512.
Mouse Resources Portal, Wellcome Trust Sanger Institute.
"International Knockout Mouse Consortium".
"Mouse Genome Informatics".
Skarnes WC, Rosen B, West AP, Koutsourakis M, Bushell W, Iyer V, Mujica AO, Thomas M, Harrow J, Cox T, Jackson D, Severin J, Biggs P, Fu J, Nefedov M, de Jong PJ, Stewart AF, Bradley A (June 2011). "A conditional knockout resource for the genome-wide study of mouse gene function". Nature. 474 (7351): 337–42. doi:10.1038/nature10163. PMC 3572410. PMID 21677750.
Dolgin E (June 2011). "Mouse library set to be knockout". Nature. 474 (7351): 262–3. doi:10.1038/474262a. PMID 21677718.
Collins FS, Rossant J, Wurst W (January 2007). "A mouse for all reasons". Cell. 128 (1): 9–13. doi:10.1016/j.cell.2006.12.018. PMID 17218247. S2CID 18872015.
van der Weyden L, White JK, Adams DJ, Logan DW (2011). "The mouse genetics toolkit: revealing function and mechanism". Genome Biology. 12 (6): 224. doi:10.1186/gb-2011-12-6-224. PMC 3218837. PMID 21722353.

SUPT7L

Model organisms

Interactions

References

Further reading