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Key Documents

SAB2500597

Sigma-Aldrich

Anti-LIS1/PAFAH1B1 antibody produced in goat

affinity isolated antibody, buffered aqueous solution

Synonym(e):

Anti-MDCR, Anti-Platelet-activating factor acetylhydrolase

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About This Item

MDL-Nummer:
MFCD01324139
UNSPSC-Code:
12352203
NACRES:
NA.41

Biologische Quelle

goat

Qualitätsniveau

100

Konjugat

unconjugated

Antikörperform

affinity isolated antibody

Antikörper-Produkttyp

primary antibodies

Klon

polyclonal

Form

buffered aqueous solution

Speziesreaktivität

human, canine, mouse, rat

Methode(n)

indirect ELISA: suitable
western blot: suitable

UniProt-Hinterlegungsnummer

P43034

Versandbedingung

dry ice

Lagertemp.

−20°C

Posttranslationale Modifikation Target

unmodified

Angaben zum Gen

human ... PAFAH1B1(5048)

Allgemeine Beschreibung

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.

Anwendung

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

Biochem./physiol. Wirkung

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.

Leistungsmerkmale und Vorteile

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.

Physikalische 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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Piktogramme

Exclamation mark
GHS07

Signalwort

Warning

H-Sätze

H315 - H319

Gefahreneinstufungen

Eye Irrit. 2 - Skin Irrit. 2

Lagerklassenschlüssel

10 - Combustible liquids

WGK

WGK 2

Flammpunkt (°F)

Not applicable

Flammpunkt (°C)

Not applicable

Analysenzertifikate (COA)

Suchen Sie nach Analysenzertifikate (COA), indem Sie die Lot-/Chargennummer des Produkts eingeben. Lot- und Chargennummern sind auf dem Produktetikett hinter den Wörtern ‘Lot’ oder ‘Batch’ (Lot oder Charge) zu finden.

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Die Dokumentenbibliothek aufrufen

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
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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