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Key Documents

SAB2500597

Sigma-Aldrich

Anti-LIS1/PAFAH1B1 antibody produced in goat

affinity isolated antibody, buffered aqueous solution

Sinonimo/i:

Anti-MDCR, Anti-Platelet-activating factor acetylhydrolase

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About This Item

Numero MDL:
MFCD01324139
Codice UNSPSC:
12352203
NACRES:
NA.41

Origine biologica

goat

Coniugato

unconjugated

Forma dell’anticorpo

affinity isolated antibody

Tipo di anticorpo

primary antibodies

Clone

polyclonal

Forma fisica

buffered aqueous solution

Reattività contro le specie

human, canine, mouse, rat

tecniche

indirect ELISA: suitable
western blot: suitable

N° accesso UniProt

P43034

Condizioni di spedizione

dry ice

Temperatura di conservazione

−20°C

modifica post-traduzionali bersaglio

unmodified

Informazioni sul gene

human ... PAFAH1B1(5048)

Descrizione generale

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.

Immunogeno

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

Applicazioni

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

Azioni biochim/fisiol

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.

Caratteristiche e vantaggi

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.

Stato fisico

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

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Pittogrammi

Exclamation mark
GHS07

Avvertenze

Warning

Indicazioni di pericolo

H315,H319

Consigli di prudenza

P305 + P351 + P338

Classi di pericolo

Eye Irrit. 2 - Skin Irrit. 2

Codice della classe di stoccaggio

10 - Combustible liquids

Classe di pericolosità dell'acqua (WGK)

WGK 2

Punto d’infiammabilità (°F)

Not applicable

Punto d’infiammabilità (°C)

Not applicable

Certificati d'analisi (COA)

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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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