Frataxin-deficient neurons and mice models of Friedreich ataxia are improved by TAT-MTScs-FXN treatment.

about

Biophysical characterisation of the recombinant human frataxin precursor.Iron in Friedreich Ataxia: A Central Role in the Pathophysiology or an Epiphenomenon?

P2860

Q52365070-E84C3731-181D-4F66-931A-1335A6159975 Q58716754-32BAFEF2-8816-4B8A-A4B3-7FACC37B4DF3

P2860

Frataxin-deficient neurons and mice models of Friedreich ataxia are improved by TAT-MTScs-FXN treatment.

Item

http://www.wikidata.org/entity/Q47693943

description

2017 nî lūn-bûn

@nan

2017年の論文

@ja

2017年学术文章

@wuu

2017年学术文章

@zh

2017年学术文章

@zh-cn

2017年学术文章

@zh-hans

2017年学术文章

@zh-my

2017年学术文章

@zh-sg

2017年學術文章

@yue

2017年學術文章

@zh-hant

name

Frataxin-deficient neurons and ...... ed by TAT-MTScs-FXN treatment.

@en

Frataxin-deficient neurons and ...... ed by TAT-MTScs-FXN treatment.

@nl

type

Item

label

Frataxin-deficient neurons and ...... ed by TAT-MTScs-FXN treatment.

@en

Frataxin-deficient neurons and ...... ed by TAT-MTScs-FXN treatment.

@nl

prefLabel

Frataxin-deficient neurons and ...... ed by TAT-MTScs-FXN treatment.

@en

Frataxin-deficient neurons and ...... ed by TAT-MTScs-FXN treatment.

@nl

P1476

Frataxin-deficient neurons and ...... ed by TAT-MTScs-FXN treatment.

@en

P2093

Anat Feldman

http://www.w3.org/2001/XMLSchema#string

Elena Britti

http://www.w3.org/2001/XMLSchema#string

Hagar Greif

http://www.w3.org/2001/XMLSchema#string

Melissa Osborne

http://www.w3.org/2001/XMLSchema#string

P2860

Role of Magmas in protein transport and human mitochondria biogenesis

Hereditary spastic paraplegia SPG13 is associated with a mutation in the gene encoding the mitochondrial chaperonin Hsp60

Pam16 has an essential role in the mitochondrial protein import motor.

Disease-Associated Mutations in the HSPD1 Gene Encoding the Large Subunit of the Mitochondrial HSP60/HSP10 Chaperonin Complex

Two-step processing of human frataxin by mitochondrial processing peptidase. Precursor and intermediate forms are cleaved at different rates

Frataxin is reduced in Friedreich ataxia patients and is associated with mitochondrial membranes

Aconitase and mitochondrial iron-sulphur protein deficiency in Friedreich ataxia

Friedreich's ataxia: autosomal recessive disease caused by an intronic GAA triplet repeat expansion

Mouse models for Friedreich ataxia exhibit cardiomyopathy, sensory nerve defect and Fe-S enzyme deficiency followed by intramitochondrial iron deposits

The in vivo mitochondrial two-step maturation of human frataxin.

P304

834-848

http://www.w3.org/2001/XMLSchema#string

P31

scholarly article

P356

10.1111/JCMM.13365

http://www.w3.org/2001/XMLSchema#string

P433

http://www.w3.org/2001/XMLSchema#string

P478

http://www.w3.org/2001/XMLSchema#string

P50

Jordi Tamarit

Joaquim Ros

Fabien Delaspre

P577

2017-10-05T00:00:00Z

http://www.w3.org/2001/XMLSchema#dateTime

P698

28980774

http://www.w3.org/2001/XMLSchema#string

P932

5783845

http://www.w3.org/2001/XMLSchema#string

Frataxin-deficient neurons and mice models of Friedreich ataxia are improved by TAT-MTScs-FXN treatment.

about

P2860

P2860

Frataxin-deficient neurons and mice models of Friedreich ataxia are improved by TAT-MTScs-FXN treatment.

description

name

type

label

prefLabel

P1433

P1476

P2093

P2860

P304

P31

P356

P433

P478

P50

P577

P698

P932

P356

P1433

P1476

P2093

P2860

P304

P31

P356

P433

P478

P50

P577

P698

P932