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SAB2500597

Sigma-Aldrich

Anti-LIS1/PAFAH1B1 antibody produced in goat

affinity isolated antibody, buffered aqueous solution

Synonym(s):

Anti-MDCR, Anti-Platelet-activating factor acetylhydrolase

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About This Item

MDL number:
UNSPSC Code:
12352203
NACRES:
NA.41

biological source

goat

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

species reactivity

human, canine, mouse, rat

technique(s)

indirect ELISA: suitable
western blot: suitable

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... PAFAH1B1(5048)

General description

PAFAH1B1 (Platelet activating factor acetyl hydrolase 1b regulatory subunit 1) encodes a protein referred to as Lis1. It is located on the chromosome location 17p13.3. The gene spans ~92 kb at the genomic level. It consists of a N-terminal coiled-coil domain and seven WD40 repeats at the C-terminus end.

Immunogen

Peptide with sequence TGSVDQTVKVWECR from the C Terminus of the protein sequence according to NP_000421.

Application

Anti-LIS1/PAFAH1B1 antibody produced in goat is suitable for indirect ELISA and western blot applications.

Biochem/physiol Actions

PAFAH1B1 (Platelet activating factor acetyl hydrolase 1b regulatory subunit 1) majorly participates in the neuronal migration pathway during brain development. It is a non-catalytic regulatory subunit of platelet activating factor (PAF) acetyl hydrolase 1b (Pafah1b) complex. During neuronal migration, it conjugates with PAFAH1B2 and PAFAH1B3 to control the concentration of platelet activating factor in the brain. Deleted gene expression of PAFAH1B1 has been reported in the 7p13.3 deletion syndrome or Miller-Dieker syndrome with mental retardation and facial dysmorphism. Heterozygous mutations of the gene cause type 1 lissencephaly characterized with impaired neuronal migration and reduction in the number of cortical gyri.

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.

Physical form

Supplied at 0.5 mg/mL in Tris saline with 0.02% sodium azide and 0.5% bovine serum albumin.

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Pictograms

Exclamation mark

Signal Word

Warning

Hazard Statements

Precautionary Statements

Hazard Classifications

Eye Irrit. 2 - Skin Irrit. 2

Storage Class Code

10 - Combustible liquids

WGK

WGK 2

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Meng-Han Tsai et al.
Acta neuropathologica, 147(1), 13-13 (2024-01-09)
The development of the cerebral cortex involves a series of dynamic events, including cell proliferation and migration, which rely on the motor protein dynein and its regulators NDE1 and NDEL1. While the loss of function in NDE1 leads to microcephaly-related
Manuel Schiff et al.
European journal of medical genetics, 53(5), 303-308 (2010-07-06)
The 17p13.3 deletion syndrome (or Miller-Dieker syndrome, MDS, MIM 247200) is characterized by lissencephaly, mental retardation and facial dysmorphism. The phenotype is attributed to haploinsufficiency of two genes present in the minimal critical region of MDS: PAFAH1B1 (formerly referred to
Andrew Kodani et al.
Neuron, 106(2), 246-255 (2020-02-26)
Genes mutated in human neuronal migration disorders encode tubulin proteins and a variety of tubulin-binding and -regulating proteins, but it is very poorly understood how these proteins function together to coordinate migration. Additionally, the way in which regional differences in
Carlos Cardoso et al.
Human mutation, 19(1), 4-15 (2001-12-26)
Classical lissencephaly (LIS) and subcortical band heterotopia (SBH) are related cortical malformations secondary to abnormal migration of neurons during early brain development. Approximately 60% of patients with classical LIS, and one patient with atypical SBH have been found to have
Amir H Assadi et al.
Neuroscience letters, 439(1), 100-105 (2008-06-03)
Reelin, an extracellular protein that signals through the Dab1 adapter protein, and Lis1 regulate neuronal migration and cellular layer formation in the brain. Loss of Reelin and reduction in Lis1 activity in mice or humans results in the disorganization of

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