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SAB3500302

Sigma-Aldrich

Anti-LIS1 antibody produced in rabbit

affinity isolated antibody, buffered aqueous solution

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Synonym(s):
Anti-Lissencephaly 1, Anti-PAFAH, Anti-Platelet-activating factor acetylhydrolase
MDL number:
MFCD03457563
UNSPSC Code:
12352203
PubChem Substance ID:
329824640
NACRES:
NA.43

biological source

rabbit

Quality Level

100

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

species reactivity

human, rat, mouse

technique(s)

immunocytochemistry: suitable
immunofluorescence: suitable
indirect ELISA: suitable
western blot: suitable

NCBI accession no.

P43034

UniProt accession no.

P43034

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

InChI

1S/C21H39O7P/c1-2-3-4-5-6-7-8-9-10-11-12-13-14-15-16-17-21(23)27-18-20(22)19-28-29(24,25)26/h6-7,9-10,20,22H,2-5,8,11-19H2,1H3,(H2,24,25,26)/b7-6+,10-9+

InChI key

ZQTAMPRZFOOEEP-AVQMFFATSA-N

Gene Information

human ... PAFAH1B1(5048)

General description

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.

Immunogen

LIS1 antibody was raised against a 14 amino acid peptide from near the carboxy terminus of human LIS1.

Application

Monoclonal Anti-LIS1 antibody produced in mouse has been used in immunofluorescence.

Biochem/physiol Actions

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.

Features and Benefits

Evaluate our antibodies with complete peace of mind. If the antibody does not perform in your application, we will issue a full credit or replacement antibody. Learn more.

Linkage

The action of this antibody can be blocked using blocking peptide SBP3500302.

Physical form

Supplied in PBS with 0.02% sodium azide.

Disclaimer

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.

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WGK

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Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Regulatory Information

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Isolation of a Miller-Dieker lissencephaly gene containing G protein beta-subunit-like repeats.
Reiner O
Nature, 364, 717-721 (1993)
T Sapir et al.
The EMBO journal, 16(23), 6977-6984 (1998-01-31)
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
Joseph M Villarin et al.
Nature communications, 7, 13865-13865 (2016-12-22)
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

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