Detail
Článek
Článek online
FT
Medvik - BMČ
  • Je něco špatně v tomto záznamu ?

Impairment of nuclear F-actin formation and its relevance to cellular phenotypes in Hutchinson-Gilford progeria syndrome

Y. Takahashi, S. Hiratsuka, N. Machida, D. Takahashi, J. Matsushita, P. Hozak, T. Misteli, K. Miyamoto, M. Harata

. 2020 ; 11 (1) : 250-263. [pub] -

Jazyk angličtina Země Spojené státy americké

Typ dokumentu časopisecké články, Research Support, N.I.H., Intramural, práce podpořená grantem, audiovizuální média

Perzistentní odkaz   https://www.medvik.cz/link/bmc21019763

Hutchinson-Gilford progeria syndrome (HGPS) is a premature aging disorder caused by a mutation of lamin A, which contributes to nuclear architecture and the spatial organization of chromatin in the nucleus. The expression of a lamin A mutant, named progerin, leads to functional and structural disruption of nuclear organization. Since progerin lacks a part of the actin-binding site of lamin A, we hypothesized that nuclear actin dynamics and function are altered in HGPS cells. Nuclear F-actin is required for the organization of nuclear shape, transcriptional regulation, DNA damage repair, and activation of Wnt/β-catenin signaling. Here we show that the expression of progerin decreases nuclear F-actin and impairs F-actin-regulated transcription. When nuclear F-actin levels are increased by overexpression of nuclear-targeted actin or by using jasplakinolide, a compound that stabilizes F-actin, the irregularity of nuclear shape and defects in gene expression can be reversed. These observations provide evidence for a novel relationship between nuclear actin and the etiology of HGPS.

Citace poskytuje Crossref.org

000      
00000naa a2200000 a 4500
001      
bmc21019763
003      
CZ-PrNML
005      
20210830101347.0
007      
ta
008      
210728s2020 xxu f 000 0|eng||
009      
AR
024    7_
$a 10.1080/19491034.2020.1815395 $2 doi
035    __
$a (PubMed)32954953
040    __
$a ABA008 $b cze $d ABA008 $e AACR2
041    0_
$a eng
044    __
$a xxu
100    1_
$a Takahashi, Yuto $u Laboratory of Molecular Biology, Graduate School of Agricultural Science, Tohoku University , Sendai, Japan
245    10
$a Impairment of nuclear F-actin formation and its relevance to cellular phenotypes in Hutchinson-Gilford progeria syndrome / $c Y. Takahashi, S. Hiratsuka, N. Machida, D. Takahashi, J. Matsushita, P. Hozak, T. Misteli, K. Miyamoto, M. Harata
520    9_
$a Hutchinson-Gilford progeria syndrome (HGPS) is a premature aging disorder caused by a mutation of lamin A, which contributes to nuclear architecture and the spatial organization of chromatin in the nucleus. The expression of a lamin A mutant, named progerin, leads to functional and structural disruption of nuclear organization. Since progerin lacks a part of the actin-binding site of lamin A, we hypothesized that nuclear actin dynamics and function are altered in HGPS cells. Nuclear F-actin is required for the organization of nuclear shape, transcriptional regulation, DNA damage repair, and activation of Wnt/β-catenin signaling. Here we show that the expression of progerin decreases nuclear F-actin and impairs F-actin-regulated transcription. When nuclear F-actin levels are increased by overexpression of nuclear-targeted actin or by using jasplakinolide, a compound that stabilizes F-actin, the irregularity of nuclear shape and defects in gene expression can be reversed. These observations provide evidence for a novel relationship between nuclear actin and the etiology of HGPS.
650    _2
$a aktiny $x genetika $x metabolismus $7 D000199
650    _2
$a zvířata $7 D000818
650    _2
$a buněčné jádro $x genetika $x metabolismus $x patologie $7 D002467
650    12
$a oprava DNA $7 D004260
650    _2
$a lidé $7 D006801
650    _2
$a lamin typ A $x genetika $x metabolismus $7 D034904
650    _2
$a myši $7 D051379
650    _2
$a buňky NIH 3T3 $7 D041681
650    _2
$a progerie $x genetika $x metabolismus $x patologie $7 D011371
650    12
$a signální dráha Wnt $7 D060449
655    _2
$a časopisecké články $7 D016428
655    _2
$a Research Support, N.I.H., Intramural $7 D052060
655    _2
$a práce podpořená grantem $7 D013485
655    _2
$a audiovizuální média $7 D059040
700    1_
$a Hiratsuka, Shogo $u Laboratory of Molecular Biology, Graduate School of Agricultural Science, Tohoku University , Sendai, Japan
700    1_
$a Machida, Nanako $u Laboratory of Molecular Biology, Graduate School of Agricultural Science, Tohoku University , Sendai, Japan
700    1_
$a Takahashi, Daisuke $u Laboratory of Molecular Biology, Graduate School of Agricultural Science, Tohoku University , Sendai, Japan
700    1_
$a Matsushita, Junpei $u Laboratory of Molecular Biology, Graduate School of Agricultural Science, Tohoku University , Sendai, Japan
700    1_
$a Hozak, Pavel $u Institute of Molecular Genetics of the Czech Academy of Sciences , Prague, Czech Republic
700    1_
$a Misteli, Tom $u National Cancer Institute, National Institutes of Health , Bethesda, MD, USA
700    1_
$a Miyamoto, Kei $u Laboratory of Molecular Developmental Biology, Faculty of Biology-Oriented Science and Technology, Kindai University , Wakayama, Japan
700    1_
$a Harata, Masahiko $u Laboratory of Molecular Biology, Graduate School of Agricultural Science, Tohoku University , Sendai, Japan
773    0_
$w MED00180459 $t Nucleus (Austin, Tex.) $x 1949-1042 $g Roč. 11, č. 1 (2020), s. 250-263
856    41
$u https://pubmed.ncbi.nlm.nih.gov/32954953 $y Pubmed
910    __
$a ABA008 $b sig $c sign $y p $z 0
990    __
$a 20210728 $b ABA008
991    __
$a 20210830101347 $b ABA008
999    __
$a ok $b bmc $g 1690550 $s 1140209
BAS    __
$a 3
BAS    __
$a PreBMC
BMC    __
$a 2020 $b 11 $c 1 $d 250-263 $e - $i 1949-1042 $m Nucleus $n Nucleus $x MED00180459
LZP    __
$a Pubmed-20210728

Najít záznam

Citační ukazatele

Možnosti archivace