D1569
Anti-Dab1 (C-terminal)
~1 mg/mL, affinity isolated antibody, buffered aqueous solution
同義詞:
Anti-Dab1, Anti-Disabled homolog 1, Anti-Yotari
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About This Item
分類程式碼代碼:
12352203
NACRES:
NA.43
共軛:
unconjugated
application:
WB
無性繁殖:
polyclonal
物種活性:
mouse, human, rat
citations:
11
技術:
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)
western blot: 2-4 μg/mL using mouse and rat brain extracts (S1 fraction)
推薦產品
生物源
rabbit
品質等級
共軛
unconjugated
抗體表格
affinity isolated antibody
抗體產品種類
primary antibodies
無性繁殖
polyclonal
形狀
buffered aqueous solution
分子量
antigen ~80 kDa
物種活性
mouse, human, rat
加強驗證
recombinant expression
Learn more about Antibody Enhanced Validation
濃度
~1 mg/mL
技術
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登錄號
運輸包裝
dry ice
儲存溫度
−20°C
目標翻譯後修改
unmodified
基因資訊
human ... DAB1(1600)
mouse ... Dab1(13131)
rat ... Dab1(266729)
一般說明
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.
應用
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.
生化／生理作用
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.
外觀
Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide.
免責聲明
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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儲存類別代碼
10 - Combustible liquids
閃點（°F）
Not applicable
閃點（°C）
Not applicable
個人防護裝備
Eyeshields, Gloves, multi-purpose combination respirator cartridge (US)
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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