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Merck
모든 사진(2)

주요 문서

D1569

Sigma-Aldrich

Anti-Dab-1 (C-terminal) from rabbit

enhanced validation

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

동의어(들):

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

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About This Item

UNSPSC 코드:
12352203
NACRES:
NA.43

생물학적 소스

rabbit

Quality Level

결합

unconjugated

항체 형태

affinity isolated antibody

항체 생산 유형

primary antibodies

클론

polyclonal

형태

buffered aqueous solution

분자량

antigen ~80 kDa

종 반응성

mouse, human, rat

향상된 검증

recombinant expression
Learn more about Antibody Enhanced Validation

농도

~1 mg/mL

기술

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)

UniProt 수납 번호

배송 상태

dry ice

저장 온도

−20°C

타겟 번역 후 변형

unmodified

유전자 정보

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

일반 설명

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.

애플리케이션

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.

생화학적/생리학적 작용

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.

물리적 형태

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

면책조항

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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Storage Class Code

10 - Combustible liquids

Flash Point (°F)

Not applicable

Flash Point (°C)

Not applicable

개인 보호 장비

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


시험 성적서(COA)

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문서 라이브러리 방문

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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