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
Items: 1 to 20 of
421
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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.
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.
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.
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.
Tämän kuvan jälkeen tiesin etsiä 9 kpl CHD- geeniä ja asetin tiedot alkuun. Viimeisellä olikin useita nimiä.
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