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SAB1305552

Anti-MAP1LC3A antibody

Name: Anti-MAP1LC3A antibody
Brand: SIGMA

mouse monoclonal, 166AT1234

别名:

MAP1 轻链 3 样蛋白 1, MAP1LC3A, 微管相关蛋白 1A/1B 轻链 3A, 自噬相关泛素样修饰物 LC3 A, 自噬相关蛋白 LC3 A

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关于此项目

UNSPSC Code:

12352203

NACRES:

NA.41

Clone:

166AT1234, monoclonal

Species reactivity:

rat, mouse, human

Application:

IF, IHC, WB

Citations:

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属性

产品名称

单克隆抗-LC3（APG8）小鼠抗, clone 166AT1234, IgG fraction of antiserum, buffered aqueous solution

biological source

mouse

Quality Level

100

antibody form

IgG fraction of antiserum

antibody product type

primary antibodies

clone

166AT1234, monoclonal

form

buffered aqueous solution

mol wt

14272 Da

species reactivity

rat, mouse, human

technique(s)

immunofluorescence: 1:25, immunohistochemistry: 1:50-1:100, western blot: 1:1000

isotype

IgG1κ

NCBI accession no.

NP_115903.1

UniProt accession no.

Q9H492

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... MAP1LC3A(84557)

说明

Physical form

以含有 0.09％（W/V）叠氮化钠的 PBS 形式提供

Disclaimer

除非我们的产品目录或产品附带的其他公司文档另有说明，否则我们的产品仅供研究使用，不得用于任何其他目的，包括但不限于未经授权的商业用途、体外诊断用途、离体或体内治疗用途或任何类型的消费或应用于人类或动物。

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存储类别

10 - Combustible liquids

flash_point_f

Not applicable

flash_point_c

Not applicable

法规信息

常规特殊物品

低风险生物材料

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Potential role of autophagy in T‑cell survival in polymyositis and dermatomyositis.

Xiaoming Shu et al.

Molecular medicine reports, 16(2), 1180-1188 (2017-06-07)

Peripheral blood T lymphocytopenia has previously been identified in polymyositis/dermatomyositis (PM/DM) patients. Therefore, the present study aimed to examine the potential role of autophagy in peripheral blood T cell survival in PM/DM patients. Transmission electron microscopy was used to detect

cPKCγ-Modulated Sequential Reactivation of mTOR Inhibited Autophagic Flux in Neurons Exposed to Oxygen Glucose Deprivation/Reperfusion.

Rongrong Hua et al.

International journal of molecular sciences, 19(5) (2018-05-08)

We have reported that conventional protein kinase Cγ (cPKCγ)-modulated neuron-specific autophagy improved the neurological outcome of mice following ischemic stroke through the Akt-mechanistic target of rapamycin (mTOR) pathway. However, its detailed molecular mechanism remains unclear. In this study, primary cortical

Phosphorylated mTORC1 represses autophagic-related mRNA translation in neurons exposed to ischemia-reperfusion injury.