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Invitrogen™ Human HSD3B1 (aa 250-285) Control Fragment Recombinant Protein
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Quantity:
100 μL
Unit Size:
100µL
Description
Highest antigen sequence indentity to the following orthologs: Mouse (83%), Rat (83%). This recombinant protein control fragment may be used for blocking experiments with the corresponding antibody, PA5-111172 (PA5-111172. In IHC/ICC and WB experiments, we recommend a 100x molar excess of the protein fragment control based on the concentration and the molecular weight. Pre-incubate the antibody-protein control fragment mixture for 30 min at room temperature.
Amyloid beta peptide (Abeta/Beta-amyloid) is the major constituent of amyloid plaques in the brains of individuals afflicted with Alzheimer's disease. Abeta peptide is 40-43 amino acids long and generated from the beta-amyloid precursor protein (beta APP) in a two-step process. The first step involves cleavage of the extracellular, amino-terminal domain of beta APP. Protein cleavage is performed by an aspartyl protease, beta-secretase (BACE) which is synthesized as a propeptide and must be modified to the mature and active form by the prohormone convertase, furin. Beta APP cleavage by the mature form of BACE results in the cellular secretion of a segment of beta APP, and a membrane-bound remnant. The remnant protein is processed by another protease, gamma-secretase. Gamma-secretase cleaves an intra-membrane site in the carboxyl-terminal domain of beta APP, thus generating the amyloid beta peptide. Gamma-secretase is believed to be a multi-subunit complex containing presenilin-1 and 2 as central components. The transmembrane glycoprotein, nicastrin, is associated with presinilins and has been found to bind to the carboxyl-terminus of beta APP and helps to modulate the production of the amyloid beta peptide. Abeta is an extracellular filamentous protein component of amyloid cores, neuritic plaques and is also found as a deposit in neurofibrillary tangles. Alzheimer's disease, the most common cause of senile dementia, is characterized by abnormal filamentous protein deposits in the brain. Beta amyloid deposits are also detected in Lewy body dementia, Down's syndrome, amyloidosis (Dutch type), cerebroarterial amyloidosis (cerebral amyloid angiopathy) and in the Guam Parkinson-Dementia complex.
Specifications
Specifications
| Accession Number | P14060 |
| Concentration | ≥5.0 mg/mL |
| For Use With (Application) | Blocking Assay, Control |
| Formulation | 1 M urea, PBS with no preservative; pH 7.4 |
| Gene ID (Entrez) | 3283 |
| Name | Human HSD3B1 (aa 250-285) Control Fragment |
| Quantity | 100 μL |
| Regulatory Status | RUO |
| Gene Alias | 3 beta-hydroxysteroid dehydrogenase 1; 3 beta-hydroxysteroid dehydrogenase/Delta 5-->4-isomerase; 3 beta-hydroxysteroid dehydrogenase/Delta 5-->4-isomerase type 1; 3 beta-hydroxysteroid dehydrogenase/Delta 5-->4-isomerase type I; 3 BETAHSD; 3-beta-HSD; 3-beta-HSD I; 3-beta-hydroxy-5-ene steroid dehydrogenase; 3-beta-hydroxy-Delta(5)-steroid dehydrogenase; 3-beta-hydroxysteroid 3-dehydrogenase; 3 BH; Delta-5-3-ketosteroid isomerase; Dihydrotestosterone oxidoreductase; HGNC:5217; HSD3B; Hsd3b1; HSDB3; HSDB3A; hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1; hydroxy-delta-MAY-steroid dehydrogenase, 3 beta- and steroid delta-isomerase; Progesterone reductase; SDR11E1; short chain dehydrogenase/reductase family 11 E, member 1; steroid Delta-isomerase; Trophoblast antigen FDO161G; unnamed protein product |
| Common Name | HSD3B1 |
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