TTR Protein is available at Gentaur for Next week delivery.
Description: Human Recombinant Transthyretin Y78F Variant Protein Filaments
Alternative Name(s): Amyloid polyneuropathy Protein, Amyloidosis I Protein, ATTR Protein, Carpal tunnel syndrome 1 Protein, CTS Protein, CTS1 Protein, HEL111 Protein, HsT2651 Protein, PALB Protein, Prealbumin Protein, Prealbumin amyloidosis type I Protein, Prealbumin Thyroxine-binding Protein, TBPA Protein, Thyroxine binding prealbumin Protein, Transthyretin Protein, TTHY_HUMAN Protein,TTR Protein
Research Area(s): Alzheimer's Disease | Axon Markers | Cell Markers | Cell Signaling | Cytoskeleton | Microtubules | MT Associated Proteins | Neurodegeneration | Neuron Markers | Neuroscience | Tangles & Tau
Accession Number: NP_000362.1
Gene ID: 7276
Applications Species: WB | SDS-PAGE | In vivo assay | In vitro assay
Expression System: E. coli
Protein Length: Full length
Amino Acid Sequence:
Purification: Ion-exchange Purified
Storage Buffer: PBS pH 7.4
Concentration: Lot/batch specific. See included datasheet.
Shipping Temperature: Dry Ice. Shipping note: Product will be shipped separately from other products purchased in the same order.
Other relevant information: For best results, sonicate immediately prior to use. Refer to the Neurodegenerative Protein Handling Instructions on our website, or on the product datasheet for further information..
Certificate of Analysis: Certified >95% pure using SDS-PAGE analysis.
Cellular Localization: Cytoplasm | Extracellular exosome | Extracellular Region | Lysosome
Scientific Background: Transthyretin is a transport protein in the serum and cerebospinal fluid that carried the thyroid hormone Thyroxine and retinol-binding protein bound to retinol. TTR misfolding and aggregation is known to be associated with the amyloiddiseases SSA, FAP and FAC (1-5). TTR is also thought to have beneficial side effects, such as binding to beta-amyloid protein, preventing beta-amyloid from accumulating into the plaques associated with Alzheimer's Disease (6). The mutant variant Y78F indicates a destabilization of the contacts between the alpha-helix and AB loop and the body of the molecule, potentially leading to applications in immne therapy for FAP (7).
References: 1. Zeldenrust S.R., Benson M.D. (2010). Wiley. pp. 795–815. 2. Westermark P., Sletten K., Johansson B., Cornwell G.G. (1990). Proc. Natl. Acad. Sci. U.S.A. 87(7): 2843–5. 3. Andrade C. (1952). Brain. 75(3): 408–27. 4. Coelho T. (1996). Curr. Opin. Neurol. 9(5): 355–9. 5. Jacobson D.R, et. al. (1997). N. Engl. J. Med. 336(7): 466–73. 6. Li X. (2011). Mol Neurodegener. 6(1):79. 7. Terazaki H.,m et al. (2006) Lab Invest. 86(1): 23-31.
Field of Use: Not for use in humans. Not for use in diagnostics or therapeutics. For research use only.
Published Species Reactivity:"