TIMM8A (1-97, His-Tag) Human Protein – AR51306PU-N | Origene

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TIMM8A (1-97, His-Tag) Human Protein – AR51306PU-N | Origene

OriGene Technologies, Inc. 9620 Medical Center Drive, Ste 200 Rockville, MD 20850, US Phone: +1-888-267-4436 [email protected] EU: [email protected] CN: [email protected] Product datasheet for AR51306PU-N TIMM8A (1-97, His-tag) Human Protein Product data: Product Type: Recombinant Proteins Description: TIMM8A (1-97, His-tag) human recombinant protein, 0.5 mg Species: Human Expression Host: E. coli Tag: His-tag Predicted MW: 13.4 kDa Concentration: lot specific Purity: >90% by SDS - PAGE Buffer: Presentation State: Purified State: Liquid purified protein Buffer System: 20 mM Tris-HCl buffer (pH 8.0) containing 0.15M NaCl, 30% glycerol, 1mM DTT Preparation: Liquid purified protein Protein Description: Recombinant human TIMM8A proten, fused to His-tag at N-terminus, was expressed in E.coli and purified by using conventional chromatography techniques. Storage: Store undiluted at 2-8°C for one week or (in aliquots) at -20°C to -80°C for longer. Avoid repeated freezing and thawing. Stability: Shelf life: one year from despatch. RefSeq: NP_001139423 Locus ID: 1678 UniProt ID: A0A2R8YDA8 Cytogenetics: Xq22.1 Synonyms: DDP; DDP1; DFN1; MTS; TIM8 This product is to be used for laboratory only. Not for diagnostic or therapeutic use. View online » ©2021 OriGene Technologies, Inc., 9620 Medical Center Drive, Ste 200, Rockville, MD 20850, US 1 / 2 TIMM8A (1-97, His-tag) Human Protein – AR51306PU-N Summary: This translocase is involved in the import and insertion of hydrophobic membrane proteins from the cytoplasm into the mitochondrial inner membrane. The gene is mutated in Mohr- Tranebjaerg syndrome/Deafness Dystonia Syndrome (MTS/DDS) and it is postulated that MTS/DDS is a mitochondrial disease caused by a defective mitochondrial protein import system. Defects in this gene also cause Jensen syndrome; an X-linked disease with opticoacoustic nerve atrophy and muscle weakness. This protein, along with TIMM13, forms a 70 kDa heterohexamer. Alternative splicing results in multiple transcript variants encoding distinct isoforms.[provided by RefSeq, Mar 2009] Protein Families: Druggable Genome Product images: This product is to be used for laboratory only. Not for diagnostic or therapeutic use. ©2021 OriGene Technologies, Inc., 9620 Medical Center Drive, Ste 200, Rockville, MD 20850, US 2 / 2.

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Identification of P.A684V Missense Mutation in the WFS1 Gene As a Frequent Cause of Autosomal Dominant Optic Atrophy and Hearing
RESEARCH ARTICLE Identiﬁcation of p.A684V Missense Mutation in the WFS1 Gene as a Frequent Cause of Autosomal Dominant Optic Atrophy and Hearing Impairment Nanna D. Rendtorff,1 Marianne Lodahl,1 Houda Boulahbel,2 Ida R. Johansen,1 Arti Pandya,3 Katherine O. Welch,4 Virginia W. Norris,4 Kathleen S. Arnos,4 Maria Bitner-Glindzicz,5 Sarah B. Emery,6 Marilyn B. Mets,7 Toril Fagerheim,8 Kristina Eriksson,9 Lars Hansen,1 Helene Bruhn,10 Claes M€oller,11 Sture Lindholm,12 Stefan Ensgaard,13 Marci M. Lesperance,6 and Lisbeth Tranebjaerg1,14*,† 1Wilhelm Johannsen Centre for Functional Genome Research, Department of Cellular and Molecular Medicine (ICMM), The Panum Institute, University of Copenhagen, Copenhagen, Denmark 2Biotech Research & Innovation Centre (BRIC), University of Copenhagen, Copenhagen, Denmark 3Department of Human and Molecular Genetics, Virginia Commonwealth University, Richmond, Virginia 4Department of Biology, Gallaudet University, Washington DC 5UCL Institute of Child Health, London, UK 6Division of Pediatric Otolaryngology, Department of Otolaryngology-Head and Neck Surgery, UniversityofMichiganHealthSystem,AnnArbor,Michigan 7Departments of Ophthalmology and Surgery, Feinberg School of Medicine, Northwestern University, Evanston, Illinois 8Division of Child and Adolescent Health, Department of Medical Genetics, University Hospital of North Norway, Tromsø, Norway 9Department of Ophthalmology, Lundby Hospital, Gothenburg, Sweden 10Division of Metabolic Diseases, Department of Laboratory Medicine, Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden 11Department of Audiology/Disability Research (SIDR), O¨rebro University, Sweden 12Department of Audiology, County Hospital, Kalmar, Sweden 13Department of Psychiatrics, Stockholm, Sweden 14Department of Audiology, Bispebjerg Hospital, Copenhagen, Denmark Received 19 July 2010; Accepted 2 February 2011 Optic atrophy (OA) and sensorineural hearing loss (SNHL) are these additional eight families.
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Dominant Optic Atrophy
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