Ubiquilin 2 (UBQLN2) Antibody

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Description
This product is currently in development. The lead time for this product may be several months. Please contact us at
Documents del producto
Product specifications
Category | Primary Antibodies |
Immunogen Target | Ubiquilin 2 (UBQLN2) |
Host | Mouse |
Reactivity | Human |
Recommended Dilution | WB: 0.01-2 µg/ml, IHC: 5-20 µg/ml, IF/ICC: 5-20 µg/ml. Optimal dilutions/concentrations should be determined by the end user. |
Clonality | Monoclonal |
Conjugation | Unconjugated |
Purification | Purified by Protein A and Protein G affinity chromatography. |
Size 1 | 1 ml |
Form | Liquid |
Tested Applications | WB, IHC, IF/ICC |
Buffer | 0.01 M PBS, pH 7.4, containing 0.05% Proclin-300, 50% glycerol. |
Availability | Please enquire. |
Storage | Aliquot and store at -20°C. Avoid repeated freeze/thaw cycles. |
Dry Ice | No |
Background | Antibody anti-UBQLN2 |
Status | RUO |
Descripción
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UBQLN2 antibody
Plays an important role in the regulation of different protein degradation mechanisms and pathways including ubiquitin-proteasome system(UPS), autophagy and the endoplasmic reticulum-associated protein degradation(ERAD) pathway. Mediates the proteasomal targeting of misfolded or accumulated proteins for degradation by binding(via UBA domain) to their polyubiquitin chains and by interacting(via ubiquitin-like domain) with the subunits of the proteasome(PubMed:10983987). Plays a role in the ERAD pathway via its interaction with ER-localized proteins FAF2/UBXD8 and HERPUD1 and may form a link between the polyubiquitinated ERAD substrates and the proteasome(PubMed:24215460, PubMed:18307982). Involved in the regulation of macroautophagy and autophagosome formation; required for maturation of autophagy-related protein LC3 from the cytosolic form LC3-I to the membrane-bound form LC3-II and may assist in the maturation of autophagosomes to autolysosomes by mediating autophagosome-lysosome fusion(PubMed:19148225, PubMed:20529957). Negatively regulates the endocytosis of GPCR receptors: AVPR2 and ADRB2, by specifically reducing the rate at which receptor-arrestin complexes concentrate in clathrin-coated pits(CCPs)(PubMed:18199683).
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