Relationship between the structure of SET/TAF-Iβ/INHAT and its histone chaperone activity

Muto, Shinsuke; Senda, Masuo; Akai, Yusuke; Sato, Lui; Suzuki, Toru; Nagai, Ryozo; Senda, Toshiya; Horikoshi, Masami

doi:10.1073/pnas.0603762104

Cited by 149 publications

(209 citation statements)

References 52 publications

Supporting

Mentioning

185

Contrasting

Unclassified

Order By: Relevance

“…Indeed, it encodes a multifunctional nuclear protein expressed in various human cell lines and tissues and involved in several pathways. 23 It interacts with SETBP1, SET-binding protein, whose haploinsufficiency had been reported in association with ID and speech delay. 24 Recently, a de novo frameshift deletion resulting in a premature stop codon in SET has been identified in a patient with congenital microcephaly, normal brain and moderate ID.…”

Section: Discussionmentioning

confidence: 99%

9q33.3q34.11 microdeletion: new contiguous gene syndrome encompassing STXBP1, LMX1B and ENG genes assessed using reverse phenotyping

et al. 2015

View full text Add to dashboard Cite

The increasing use of array-CGH in malformation syndromes with intellectual disability could lead to the description of new contiguous gene syndrome by the analysis of the gene content of the microdeletion and reverse phenotyping. Thanks to a national and international call for collaboration by Achropuce and Decipher, we recruited four patients carrying de novo overlapping deletions of chromosome 9q33.3q34.11, including the STXBP1, the LMX1B and the ENG genes. We restrained the selection to these three genes because the effects of their haploinsufficency are well described in the literature and easily recognizable clinically. All deletions were detected by array-CGH and confirmed by FISH. The patients display common clinical features, including intellectual disability with epilepsy, owing to the presence of STXBP1 within the deletion, nail dysplasia and bone malformations, in particular patellar abnormalities attributed to LMX1B deletion, epistaxis and cutaneousmucous telangiectasias explained by ENG haploinsufficiency and common facial dysmorphism. This systematic analysis of the genes comprised in the deletion allowed us to identify genes whose haploinsufficiency is expected to lead to disease manifestations and complications that require personalized follow-up, in particular for renal, eye, ear, vascular and neurological manifestations.

show abstract

Section: Discussionmentioning

confidence: 99%

9q33.3q34.11 microdeletion: new contiguous gene syndrome encompassing STXBP1, LMX1B and ENG genes assessed using reverse phenotyping

et al. 2015

View full text Add to dashboard Cite

show abstract

“…The N-terminal 24 amino acids of human SET/ TAF-I are not required for many activities such as DNA replication and transcription stimulation (Miyaji-Yamaguchi et al, 1999), but the residues Thr23 and Ser24 are involved in a long -helix ( 2) which has a stable structure in the crystal structure of SET/TAF-I ÁC (PDB code 2e50; Muto et al, 2007). Therefore, a truncated form of SET/TAF-I was designed for crystallization experiments that lacked 22 residues from the N-terminus.…”

Section: Resultsmentioning

confidence: 99%

“…Molecular replacement was carried out with MOLREP (Vagin & Teplyakov, 1997) in the CCP4 suite (Collaborative Computational Project, Number 4, 1994) using the structure of residues 23-225 of H. sapiens SET/TAF-I ÁC (PDB code 2e50; Muto et al, 2007) as a search model. Furthermore, systematic absences indicated that the SET/TAF-I ÁN crystal belonged to space group P4 3 2 1 2 or its enantiomer P4 1 2 1 2.…”

Section: Resultsmentioning

confidence: 99%

“…All of those proteins contain the NAP domain. The crystal structure of human SET/TAF-I ÁC (residues 1-225) has also been reported (PDB code 2e50; Muto et al, 2007). Despite the fact that the C-terminal acidic domain may be disordered, it is presumed that this domain may influence the structure of SET/TAF-I .…”

Section: Introductionmentioning

confidence: 99%

“…The C-terminal acidic domain is required for DNA-replication and transcriptionstimulatory activity (Kawase et al, 1996). Although it has been reported that the C-terminal acidic stretch of SET/TAF-I is not necessary for its binding activity to histone H3 and H4, it is required for histone H2A-H2B binding activity (Muto et al, 2007). Full-length SET/TAF-I inhibits histone acetylation.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Cloning, purification, crystallization and preliminary X-ray crystallographic analysis of SET/TAF-Iβ ΔN fromHomo sapiens

Yang

Shi

et al. 2010

Acta Cryst Sect F

View full text Add to dashboard Cite

The histone chaperone SET encoded by the SET gene, which is also known as template-activating factor I (TAF-I), is a multifunctional molecule that is involved in many biological phenomena such as histone binding, nucleosome assembly, chromatin remodelling, replication, transcription and apoptosis. A truncated SET/TAF-I ÁN protein that lacked the first 22 residues of the N-terminus but contained the C-terminal acidic domain and an additional His 6 tag at the C-terminus was overexpressed in Escherichia coli and crystallized by the hanging-drop vapour-diffusion method using sodium acetate as precipitant at 283 K. The crystals diffracted to 2.7 Å resolution and belonged to space group P4 3 2 1 2.

show abstract

New moonlighting functions of mitochondrial cytochrome c in the cytoplasm and nucleus

et al. 2019

View full text Add to dashboard Cite

Cytochrome c (Cc) is a protein that functions as an electron carrier in the mitochondrial respiratory chain. However, Cc has moonlighting roles outside mitochondria driving the transition of apoptotic cells from life to death. When living cells are damaged, Cc escapes its natural mitochondrial environment and, once in the cytosol, it binds other proteins to form a complex named the apoptosome—a platform that triggers caspase activation and further leads to controlled cell dismantlement. Early released Cc also binds to inositol 1,4,5‐triphosphate receptors on the ER membrane, which stimulates further massive Cc release from mitochondria. Besides the well‐characterized binding proteins contributing to the proapoptotic functions of Cc, many novel protein targets have been recently described. Among them, histone chaperones were identified as key partners of Cc following DNA breaks, indicating that Cc might modulate chromatin dynamics through competitive binding to histone chaperones. In this article, we review the ample set of recently discovered antiapoptotic proteins—involved in DNA damage, transcription, and energetic metabolism—reported to interact with Cc in the cytoplasm and even the nucleus upon DNA breaks.

show abstract

Relationship between the structure of SET/TAF-Iβ/INHAT and its histone chaperone activity

Cited by 149 publications

References 52 publications

9q33.3q34.11 microdeletion: new contiguous gene syndrome encompassing STXBP1, LMX1B and ENG genes assessed using reverse phenotyping

9q33.3q34.11 microdeletion: new contiguous gene syndrome encompassing STXBP1, LMX1B and ENG genes assessed using reverse phenotyping

Cloning, purification, crystallization and preliminary X-ray crystallographic analysis of SET/TAF-Iβ ΔN fromHomo sapiens

New moonlighting functions of mitochondrial cytochrome c in the cytoplasm and nucleus

Contact Info

Product

Resources

About