The gene PAFAH1B1 (platelet activating factor acetylhydrolase 1b regulatory subunit 1) encodes a protein named LIS1 (lissencephaly-1) that forms the α subunit of the intracellular Ib isoform of platelet-activating factor acteylhydrolase (PAFAH). The gene is mapped to human chromosome 17p13.3.
免疫原
LIS1 antibody was raised against a 14 amino acid peptide from near the carboxy terminus of human LIS1.
アプリケーション
Monoclonal Anti-LIS1 antibody produced in mouse has been used in immunofluorescence.[1]
生物化学的/生理学的作用
The heterotrimeric enzyme, platelet-activating factor acteylhydrolase (PAFAH), catalyzes the cleavage of acetyl group at the SN-2 position of platelet-activating factor. The α subunit encoded by the gene PAFAH1B1 (platelet activating factor acetylhydrolase 1b regulatory subunit 1) interacts with tubulin and affects microtubule dynamics. Mutations in this gene have been linked to Miller–Dieker lissencephaly, a human brain malformation characterized by a smooth cerebral surface and a disordered organization of the cortical layers resulting from a defect in neuronal migration.
特徴および利点
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関連事項
The action of this antibody can be blocked using blocking peptide SBP3500302.
物理的形状
PBS(0.02% アジ化ナトリウム含有)
免責事項
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
Forming the structure of the human brain involves extensive neuronal migration, a process dependent on cytoskeletal rearrangement. Neuronal migration is believed to be disrupted in patients exhibiting the developmental brain malformation lissencephaly. Previous studies have shown that LIS1, the defective
Cytoplasmic dynein mediates retrograde transport in axons, but it is unknown how its transport characteristics are regulated to meet acutely changing demands. We find that stimulus-induced retrograde transport of different cargos requires the local synthesis of different dynein cofactors. Nerve