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Merck
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重要文件

WH0001641M1

Sigma-Aldrich

Monoclonal Anti-DCX antibody produced in mouse

clone 1G12, purified immunoglobulin, buffered aqueous solution

同義詞:

Anti-DBCN, Anti-DC, Anti-LISX, Anti-SCLH, Anti-XLIS, Anti-doublecortex; lissencephaly, X-linked (doublecortin)

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About This Item

MDL號碼:
分類程式碼代碼:
12352203
NACRES:
NA.41

生物源

mouse

品質等級

共軛

unconjugated

抗體表格

purified immunoglobulin

抗體產品種類

primary antibodies

無性繁殖

1G12, monoclonal

形狀

buffered aqueous solution

物種活性

human

技術

immunofluorescence: suitable
indirect ELISA: suitable
western blot: 1-5 μg/mL

同型

IgG1κ

GenBank登錄號

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 ... DCX(1641)

一般說明

In the developing cortex, cortical neurons must migrate over long distances to reach the site of their final differentiation. The protein encoded by this gene is a cytoplasmic protein which appears to direct neuronal migration by regulating the organization and stability of microtubules. The encoded protein contains two doublecortin domains, which bind microtubules. In addition, the encoded protein interacts with LIS1, the regulatory gamma subunit of platelet activating factor acetyl hydrolase, and this interaction is important to proper microtubule function in the developing cortex. Mutations in this gene are a cause of X-linked lissencephaly. Multiple transcript variants encoding at least three different isoforms have been found for this gene. (provided by RefSeq) Doublecortin (DCX) is an essential gene for neurodevelopment and is expressed in neuronal progenitor cells and immature migrating neurons in the foetus. DCX is mapped to human chromosome Xq22.3-q23.

免疫原

DCX (AAH27925, 1 a.a. ~ 360 a.a) full-length recombinant protein with GST tag. MW of the GST tag alone is 26 KDa.

Sequence
MELDFGHFDERDKTSRNMRGSRMNGLPSPTHSAHCSFYRTRTLQALSNEKKAKKVRFYRNGDRYFKGIVYAVSSDRFRSFDALLADLTRSLSDNINLPQGVRYIYTIDGSRKIGSMDELEEGESYVCSSDNFFKKVEYTKNVNPNWSVNVKTSANMKAPQSLASSNSAQARENKDFVRPKLVTIIRSGVKPRKAVRVLLNKKTAHSFEQVLTDITEAIKLETGVVKKLYTLDGKQVTCLHDFFGDDDVFIACGPEKFRYAQDDFSLDENECRVMKGNPSATAGPKASPTPQKTSAKSPGPMRRSKSPADSANGTSSSQLSTPKSKQSPISTPTSPGSLRKHKDLYLPLSLDDSDSLGDSM

生化/生理作用

Doublecortin (DCX) encodes a protein which binds to microtubule and is involved in neuronal migration through Ca2+ signalling. Mutations in DCX causes defect in neuronal migration, that results in lissencephaly (LIS) or smooth brain in males, and in females, it leads to subcortical laminar heterotopia (SCLH).LIS/SCLH leads to mental retardation or epilepsy.

外觀

Solution in phosphate buffered saline, pH 7.4

法律資訊

GenBank is a registered trademark of United States Department of Health and Human Services

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)


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分析證明 (COA)

Lot/Batch Number

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存取文件庫

Mutation analysis of the DCX gene and genotype/phenotype correlation in subcortical band heterotopia
Matsumoto N, et al.
European Journal of Human Genetics, 9(1), 5-12 (2001)
Human doublecortin (DCX) and the homologous gene in mouse encode a putative Ca2+-dependent signaling protein which is mutated in human X-linked neuronal migration defects
Sossey-Alaoui K, et al.
Human Molecular Genetics, 7(8), 1327-1332 (1998)
Spatio-temporal transcriptome of the human brain
Kang HJ, et al.
Nature, 478(7370), 483-489 (2011)
Evidence for tangential migration disturbances in human lissencephaly resulting from a defect in LIS1, DCX and ARX genes
Marcorelles P, et al.
Acta Neuropathologica, 120(4), 503-515 (2010)
Dcx reexpression reduces subcortical band heterotopia and seizure threshold in an animal model of neuronal migration disorder
Manent JB, et al.
Nature Medicine, 15(1), 84-90 (2009)

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