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Documenti fondamentali

D1569

Sigma-Aldrich

Anti-Dab1 (C-terminal)

enhanced validation

~1 mg/mL, affinity isolated antibody, buffered aqueous solution

Sinonimo/i:

Anti-Dab1, Anti-Disabled homolog 1, Anti-Yotari

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About This Item

Codice UNSPSC:
12352203
NACRES:
NA.43

Origine biologica

rabbit

Livello qualitativo

Coniugato

unconjugated

Forma dell’anticorpo

affinity isolated antibody

Tipo di anticorpo

primary antibodies

Clone

polyclonal

Forma fisica

buffered aqueous solution

PM

antigen ~80 kDa

Reattività contro le specie

mouse, human, rat

Convalida avanzata

recombinant expression
Learn more about Antibody Enhanced Validation

Concentrazione

~1 mg/mL

tecniche

western blot: 2-4 μg/mL using HEK-293T cells expressing human DAB1
western blot: 2-4 μg/mL using mouse and rat brain extracts (S1 fraction)

N° accesso UniProt

Condizioni di spedizione

dry ice

Temperatura di conservazione

−20°C

modifica post-traduzionali bersaglio

unmodified

Informazioni sul gene

human ... DAB1(1600)
mouse ... Dab1(13131)
rat ... Dab1(266729)

Descrizione generale

Disabled-1 is an intracellular adaptor protein that belongs to the Reelin signaling pathway. The amino terminus of Dab1 contains a phosphotyrosine-binding (PTB) domain. The domain interacts with NPXY sequences within the cytoplasmic regions of several membrane-bound proteins including lipoprotein receptors and amyloid precursor protein (APP) family.

Applicazioni

Anti-Dab-1 (C-terminal) was used at a working dilution of 1:2000 to probe the protein sample extracted from brain tissue of mice by western blotting in a study.

Azioni biochim/fisiol

Dab1 plays a key role during brain development by controlling neuronal positioning as well as modulation of long-term potentiation (LTP) in the adult brain. Tyrosine phosphorylation of Dab1 is triggered by the binding of reelin to the lipoprotein receptors Apolipoprotein E receptor 2 (ApoER2) and the very low density lipoprotein receptor (VLDLR), thus initiating a signaling cascade that includes the Src-family kinases and Akt.

Stato fisico

Solution in 0.01 M phos­phate buffered saline, pH 7.4, containing 15 mM sodium azide.

Esclusione di responsabilità

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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Codice della classe di stoccaggio

10 - Combustible liquids

Punto d’infiammabilità (°F)

Not applicable

Punto d’infiammabilità (°C)

Not applicable

Dispositivi di protezione individuale

Eyeshields, Gloves, multi-purpose combination respirator cartridge (US)


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Danielle E Whittaker et al.
The Journal of clinical investigation, 127(3), 874-887 (2017-02-07)
The mechanisms underlying the neurodevelopmental deficits associated with CHARGE syndrome, which include cerebellar hypoplasia, developmental delay, coordination problems, and autistic features, have not been identified. CHARGE syndrome has been associated with mutations in the gene encoding the ATP-dependent chromatin remodeler
B W Howell et al.
The EMBO journal, 16(1), 121-132 (1997-01-02)
Here, we identify a mouse homolog of the Drosophila Disabled (Dab) protein, mDab1, and show it is an adaptor molecule functioning in neural development. We find that mDab1 is expressed in certain neuronal and hematopoietic cell lines, and is localized
B W Howell et al.
Current biology : CB, 10(15), 877-885 (2000-08-26)
The extracellular protein Reln controls neuronal migrations in parts of the cortex, hippocampus and cerebellum. In vivo, absence of Reln correlates with up-regulation of the docking protein Dab1 and decreased Dab1 tyrosine phosphorylation. Loss of the Reln receptor proteins, apolipoprotein
T Hiesberger et al.
Neuron, 24(2), 481-489 (1999-11-26)
The large extracellular matrix protein Reelin is produced by Cajal-Retzius neurons in specific regions of the developing brain, where it controls neuronal migration and positioning. Genetic evidence suggests that interpretation of the Reelin signal by migrating neurons involves two neuronal
Giampiero Palladino et al.
Journal of molecular neuroscience : MN, 61(3), 359-367 (2016-11-21)
Recent evidence highlights the protective role of reelin against amyloid β (Aβ)-induced synaptic dysfunction and cognitive impairment in Alzheimer disease (AD). In this study, exploiting TgCRND8 mice that overexpress a mutant form of amyloid β precursor protein (AβPP) and display

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