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torsdag 16 maj 2019

DNA.ta sitovat Kromodomaaninhelikaasit CHD1- CHD9

 Kromodomaanihelikaasit, jotka sitovat DNA:ta

CHD1- CHD9
CHD1, PILBOS (5q15-q21.1), https://www.ncbi.nlm.nih.gov/gene/1105
CHD2,EEOC (15q26.1) , https://www.ncbi.nlm.nih.gov/gene/1106
CHD3, Mi-2-ALPHA, Zinc finger helicase ZFH (17p13.1), https://www.ncbi.nlm.nih.gov/gene/1107
CHD4, Mi-2-BETA, SHIHIWES  (12p13.31) , https://www.ncbi.nlm.nih.gov/gene/1108
CHD5, (1p36.31) neuronispesifinen tuumorisuppressori.  https://www.ncbi.nlm.nih.gov/gene/26038
CHD6, RIGB (20q12), radiation induced gene B, https://www.ncbi.nlm.nih.gov/gene/84181
CHD7,CRG, HH%,US3,KAL5,(8q12.2)   https://www.ncbi.nlm.nih.gov/gene/55636
CHD8, AUTS18, HELSNF1, (14q11.2)  https://www.ncbi.nlm.nih.gov/gene/57680

CHD9, AD013, CDeMM, KISH2, PRIC320,(16q12.2) https://www.ncbi.nlm.nih.gov/gene/80205 Preferred Names, chromodomain-helicase-DNA-binding protein 9; Names ATP-dependent helicase CHD9; PPAR-alpha-interacting complex protein 320 kDa, PPAR{gamma}-interacting cofactor 320 kDa, chromatin remodeling factor CHROM1, chromatin-related mesenchymal modulator, ciprofibrate bound protein p240, kismet homolog 2, peroxisomal proliferator-activated receptor A-interacting complex 320 kDa protein,  proteinx0008.

...

CHRomatinOrganization MOdifier , CHROMO
Chromo domain, mikä se on? Se on  proteiinissa oleva domeeni, joka vaikuttaa kromatiiniin.
Alustavaa tietoa luomakunnan ”chromodomain (CD) containig proteins”- aivan kasvikunnasta ihmiseen tässä koeeläimellä hiirellä tehdyssä työssä:

Göteborgin Biomedisiinisessä Kirjastossa 14.5. 2019 oli esitteillä väitöskirjatyö: Susanna Larsson: Cell-based models for studying paediatric high-grade gliomas. Väitöstilaisuus on edessäpäin.
Katselin johdantoa ja kirjassa mainittujen termien luetteloa. Histonimodifikaation yhteydessä oli tekstissä prosessoivista tekijöistä (Histone modification, ... processed by writers , and executed by epigenetic readers ... chromodomain, tudordomain and bromodomain containing proteins which help to interpret the modification) -

Huomasin , että tietoni näistä domaaneista oli vähäinen. Bromodomeeni on tosin ilmentynyt lukemissani TRIM-proteiineissa ja joissain yhteyksissä olen havainnut chromodomeenia. Tudordomeenista en tiennyt mitään. joten tänään katson näitä kolmea domeenia sisältäviä ihmisen proteiineja PubMed lähteestä ja nettiartikkeleista.

Chromodomeenista löysin yllä mainitsemani laajan työn, joka oli tehty hiirellä, ja työssä mainittiin myös luomakunnan muita organismeja: kasvi, virus, hiiva ja sitten myös ihmisen vastaava kromodomaaniproteiinia sisältävä proteiinijoukko lyhyesti. Hiiren ja ihmisen kromodomaaneista suurin osa oli samanlaisia, mutta ihmisellä on muutamia kromodomaaneja, joita hiiressä ei esiinny ja hiiressä taas joitain, joita ihmisessä ei esiinny. 
 
LÄHDE: Genome Res. 2003 Jun; 13(6b): 1416–1429.
doi: 10.1101/gr.1015703 PMCID: PMC403676 PMID: 12819141
Identification and Analysis of Chromodomain-Containing Proteins Encoded in the Mouse Transcriptome Khairina Tajul-Arifin,1 Rohan Teasdale,1 Timothy Ravasi,1 David A. Hume,1,2 RIKEN GER Group3, GSL Members4,5, and John S. Mattick1,

Etsin nyt PubMed- lähteestä ainoastaan ihmisen kromodomaaniproteiineista ja geeneistä tietoa. Aivan tämän vuoden artikkeleita oli neljä ja ne esittivät geenit CHD6, CHD7, ja CHD8

Ihmisen CHROMODOMAIN proteiinit
”Human Chromodomain Proteins” PubMed
Search results
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Select item 309179131.

Dahiya R, Naqvi AAT, Mohammad T, Alajmi MF, Rehman MT, Hussain A, Hassan MI.
Int J Biol Macromol. 2019 Jun 15;131:1101-1116. doi: 10.1016/j.ijbiomac.2019.03.162. Epub 2019 Mar 24.
Abstract
Epigenetic readers are specific proteins which recognize histone marks and represents the underlying mechanism for chromatin regulation. Histone H3 lysine methylation is a potential epigenetic code for the chromatin organization and transcriptional control. Recognition of histone methylation is achieved by evolutionary conserved reader modules known as chromodomain, identified in several proteins, and is involved in transcriptional silencing and chromatin remodelling. Genetic perturbations within the structurally conserved chromodomain could potentially mistarget the reader protein and impair their regulatory pathways, ultimately leading to cellular chaos by setting the stage for tumor development and progression. Here, we report the structural conservations associated with diverse functions, prognostic significance and functional consequences of mutations within chromodomain (CD) of human proteins in distinct cancers. We have extensively analysed chromodomain containing human proteins in terms of their structural-functional ability to act as a molecular switch in the recognition of methyl-lysine recognition. We further investigated the combinatorial potential, target promiscuity and binding specificity associated with their underlying mechanisms. Indeed, the molecular mechanism of epigenetic silencing significantly underlies a newer cancer therapy approach. We hope that a critical understanding of chromodomains will pave the way for novel paths of research providing newer insights into the designing of effective anti-cancer therapies.

Select item 308506782.
Machado RAC, Schneider H, DeOcesano-Pereira C, Lichtenstein F, Andrade F, Fujita A, Trombetta-Lima M, Weller M, Bowman-Colin C, Sogayar MC.
Sci Rep. 2019 Mar 8;9(1):3952. doi: 10.1038/s41598-019-39564-w.
Abstract
Chromatin remodeler proteins exert an important function in promoting dynamic modifications in the chromatin architecture, performing a central role in regulating gene transcription. Deregulation of these molecular machines may lead to striking perturbations in normal cell function. The CHD7 gene is a member of the chromodomain helicase DNA-binding family and, when mutated, has been shown to be the cause of the CHARGE syndrome, a severe developmental human disorder. Moreover, CHD7 has been described to be essential for neural stem cells and it is also highly expressed or mutated in a number of human cancers. However, its potential role in glioblastoma has not yet been tested. Here, we show that CHD7 is up-regulated in human glioma tissues and we demonstrate that CHD7 knockout (KO) in LN-229 glioblastoma cells suppresses anchorage-independent growth and spheroid invasion in vitro. Additionally, CHD7 KO impairs tumor growth and increases overall survival in an orthotopic mouse xenograft model. Conversely, ectopic overexpression of CHD7 in LN-428 and A172 glioblastoma cell lines increases cell motility and invasiveness in vitro and promotes LN-428 tumor growth in vivo. Finally, RNA-seq analysis revealed that CHD7 modulates a specific transcriptional signature of invasion-related target genes. Further studies should explore clinical-translational implications for glioblastoma treatment.
 
Select item 306929113.
Wade AA, Lim K, Catta-Preta R, Nord AS.
Front Mol Neurosci. 2019 Jan 14;11:481. doi: 10.3389/fnmol.2018.00481. eCollection 2018.
Abstract
The packaging of DNA into chromatin determines the transcriptional potential of cells and is central to eukaryotic gene regulation. Case sequencing studies have revealed mutations to proteins that regulate chromatin state, known as chromatin remodeling factors, with causal roles in neurodevelopmental disorders. Chromodomain helicase DNA binding protein 8 (CHD8) encodes a chromatin remodeling factor with among the highest de novo loss-of-function mutation rates in patients with autism spectrum disorder (ASD). However, mechanisms associated with CHD8 pathology have yet to be elucidated. We analyzed published transcriptomic data across CHD8 in vitro and in vivo knockdown and knockout models and CHD8 binding across published ChIP-seq datasets to identify convergent mechanisms of gene regulation by CHD8. Differentially expressed genes (DEGs) across models varied, but overlap was observed between downregulated genes involved in neuronal development and function, cell cycle, chromatin dynamics, and RNA processing, and between upregulated genes involved in metabolism and immune response. Considering the variability in transcriptional changes and the cells and tissues represented across ChIP-seq analysis, we found a surprisingly consistent set of high-affinity CHD8 genomic interactions. CHD8 was enriched near promoters of genes involved in basic cell functions and gene regulation. Overlap between high-affinity CHD8 targets and DEGs shows that reduced dosage of CHD8 directly relates to decreased expression of cell cycle, chromatin organization, and RNA processing genes, but only in a subset of studies. This meta-analysis verifies CHD8 as a master regulator of gene expression and reveals a consistent set of high-affinity CHD8 targets across human, mouse, and rat in vivo and in vitro studies. These conserved regulatory targets include many genes that are also implicated in ASD. Our findings suggest a model where perturbation to dosage-sensitive CHD8 genomic interactions with a highly-conserved set of regulatory targets leads to model-specific downstream transcriptional impacts.

Select item 306515624.
Moore S, Berger ND, Luijsterburg MS, Piett CG, Stanley FKT, Schräder CU, Fang S, Chan JA, Schriemer DC, Nagel ZD, van Attikum H, Goodarzi AA.
Nat Commun. 2019 Jan 16;10(1):241. doi: 10.1038/s41467-018-08111-y.
Abstract
Cell survival after oxidative DNA damage requires signaling, repair and transcriptional events often enabled by nucleosome displacement, exchange or removal by chromatin remodeling enzymes. Here, we show that Chromodomain Helicase DNA-binding protein 6 (CHD6), distinct to other CHD enzymes, is stabilized during oxidative stress via reduced degradation. CHD6 relocates rapidly to DNA damage in a manner dependent upon oxidative lesions and a conserved N-terminal poly(ADP-ribose)-dependent recruitment motif, with later retention requiring the double chromodomain and central core. CHD6 ablation increases reactive oxygen species persistence and impairs anti-oxidant transcriptional responses, leading to elevated DNA breakage and poly(ADP-ribose) induction that cannot be rescued by catalytic or double chromodomain mutants. Despite no overt epigenetic or DNA repair abnormalities, CHD6 loss leads to impaired cell survival after chronic oxidative stress, abnormal chromatin relaxation, amplified DNA damage signaling and checkpoint hypersensitivity. We suggest that CHD6 is a key regulator of the oxidative DNA damage response.

Muistiin 16.5. 2019 
Ps. 
Löysin hyvän kuvankin ihmisen DNA:ta sitovista kromodomaanihelikaasiproteiineista
Chromodomain Helicase DNA-binding family 

https://www.ncbi.nlm.nih.gov/core/lw/2.0/html/tileshop_pmc/tileshop_pmc_inline.html?title=Click%20on%20image%20to%20zoom&p=PMC3&id=4390162_fig-1.jpg
Tämän kuvan jälkeen tiesin etsiä 9 kpl CHD-  geeniä ja asetin tiedot  alkuun.  Viimeisellä olikin useita nimiä.














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