Characterization of seipin/BSCL2, a protein associated with spastic paraplegia 17.
about
Neuronal seipin knockout facilitates Aβ-induced neuroinflammation and neurotoxicity via reduction of PPARγ in hippocampus of mouseLack of testicular seipin causes teratozoospermia syndrome in men.Hereditary spastic paraplegia: clinico-pathologic features and emerging molecular mechanisms.Alternative splicing of Spg7, a gene involved in hereditary spastic paraplegia, encodes a variant of paraplegin targeted to the endoplasmic reticulum.Neuroanatomical characterisation of the expression of the lipodystrophy and motor-neuropathy gene Bscl2 in adult mouse brainSeipin mutation at glycosylation sites activates autophagy in transfected cells via abnormal large lipid droplets generation.Molecular characterization of seipin and its mutants: implications for seipin in triacylglycerol synthesis.Segregated responses of mammary gland development and vaginal opening to prepubertal genistein exposure in Bscl2(-/-) female mice with lipodystrophy.Seipin: from human disease to molecular mechanismSeipin knockout in mice impairs stem cell proliferation and progenitor cell differentiation in the adult hippocampal dentate gyrus via reduced levels of PPARγ.Motor neuron degeneration in a mouse model of seipinopathy.The human lipodystrophy protein seipin is an ER membrane adaptor for the adipogenic PA phosphatase lipin 1.Lipodystrophies: disorders of adipose tissue biology.Analysis of naturally occurring mutations in the human lipodystrophy protein seipin reveals multiple potential pathogenic mechanismsRe-analysis of an original CMTX3 family using exome sequencing identifies a known BSCL2 mutation.Molecular mechanisms controlling human adipose tissue development: insights from monogenic lipodystrophies.Alleviation of seipinopathy-related ER stress by triglyceride storage.Autophagy as an Emerging Common Pathomechanism in Inherited Peripheral Neuropathies.Seipin oligomers can interact directly with AGPAT2 and lipin 1, physically scaffolding critical regulators of adipogenesisWhole Exome Sequencing Reveals a BSCL2 Mutation Causing Progressive Encephalopathy with Lipodystrophy (PELD) in an Iranian Pediatric Patient.A Patient with Congenital Generalized Lipodystrophy Due To a Novel Mutation in BSCL2: Indications for Secondary Mitochondrial Dysfunction.A new seipin-associated neurodegenerative syndrome.Characterization of alternative isoforms and inclusion body of the TAR DNA-binding protein-43.Evidence of a link between ubiquilin 2 and optineurin in amyotrophic lateral sclerosis.Lack of seipin in neurons results in anxiety- and depression-like behaviors via down regulation of PPARγ.The expression of SEIPIN in the mouse central nervous system.Nuclear transport impairment of amyotrophic lateral sclerosis-linked mutations in FUS/TLS.Seipin deficiency in mice causes loss of dopaminergic neurons via aggregation and phosphorylation of α-synuclein and neuroinflammation.Exploring Seipin: From Biochemistry to Bioinformatics PredictionsImpairment of respiratory muscle strength in Berardinelli-Seip congenital lipodystrophy subjects
P2860
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P2860
Characterization of seipin/BSCL2, a protein associated with spastic paraplegia 17.
description
2008 nî lūn-bûn
@nan
2008年の論文
@ja
2008年学术文章
@wuu
2008年学术文章
@zh-cn
2008年学术文章
@zh-hans
2008年学术文章
@zh-my
2008年学术文章
@zh-sg
2008年學術文章
@yue
2008年學術文章
@zh
2008年學術文章
@zh-hant
name
Characterization of seipin/BSCL2, a protein associated with spastic paraplegia 17.
@en
Characterization of seipin/BSCL2, a protein associated with spastic paraplegia 17.
@nl
type
label
Characterization of seipin/BSCL2, a protein associated with spastic paraplegia 17.
@en
Characterization of seipin/BSCL2, a protein associated with spastic paraplegia 17.
@nl
prefLabel
Characterization of seipin/BSCL2, a protein associated with spastic paraplegia 17.
@en
Characterization of seipin/BSCL2, a protein associated with spastic paraplegia 17.
@nl
P1476
Characterization of seipin/BSCL2, a protein associated with spastic paraplegia 17.
@en
P2093
Hiroshi Iida
Taishi Fujisawa
P304
P356
10.1016/J.NBD.2008.05.004
P577
2008-05-22T00:00:00Z