Differential recruitment of UBQLN2 to nuclear inclusions in the polyglutamine diseases HD and SCA3.
about
Sequestration of cellular interacting partners by protein aggregates: implication in a loss-of-function pathology.Profilin reduces aggregation and phase separation of huntingtin N-terminal fragments by preferentially binding to soluble monomers and oligomers.Mutant UBQLN2 promotes toxicity by modulating intrinsic self-assembly
P2860
Differential recruitment of UBQLN2 to nuclear inclusions in the polyglutamine diseases HD and SCA3.
description
2015 nî lūn-bûn
@nan
2015年の論文
@ja
2015年学术文章
@wuu
2015年学术文章
@zh-cn
2015年学术文章
@zh-hans
2015年学术文章
@zh-my
2015年学术文章
@zh-sg
2015年學術文章
@yue
2015年學術文章
@zh
2015年學術文章
@zh-hant
name
Differential recruitment of UB ...... lutamine diseases HD and SCA3.
@ast
Differential recruitment of UB ...... lutamine diseases HD and SCA3.
@en
type
label
Differential recruitment of UB ...... lutamine diseases HD and SCA3.
@ast
Differential recruitment of UB ...... lutamine diseases HD and SCA3.
@en
prefLabel
Differential recruitment of UB ...... lutamine diseases HD and SCA3.
@ast
Differential recruitment of UB ...... lutamine diseases HD and SCA3.
@en
P2093
P2860
P1476
Differential recruitment of UB ...... lutamine diseases HD and SCA3.
@en
P2093
Biswarathan Ramani
Eiko N Minakawa
Henry L Paulson
Maria do Carmo Costa
Matthew D Perkins
Roger L Albin
Sara J Tallaksen-Greene
Sean A Merillat
P2860
P304
P356
10.1016/J.NBD.2015.06.017
P577
2015-06-30T00:00:00Z