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SAB1305552

Sigma-Aldrich

MONOCLONAL ANTI-LC3 (APG8) antibody produced in mouse

clone 166AT1234, IgG fraction of antiserum, buffered aqueous solution

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Synonym(s):
Autophagy-related protein LC3 A, Autophagy-related ubiquitin-like modifier LC3 A, MAP1 light chain 3-like protein 1, MAP1LC3A, Microtubule-associated proteins 1A/1B light chain 3A
NACRES:
NA.41

biological source

mouse

Quality Level

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.

UniProt accession no.

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

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This Item
SAB1305638SAB1306611SAB1305635
antibody form

IgG fraction of antiserum

antibody form

IgG fraction of antiserum

antibody form

purified immunoglobulin

antibody form

purified immunoglobulin

clone

166AT1234, monoclonal

clone

polyclonal

clone

polyclonal

clone

polyclonal

form

buffered aqueous solution

form

buffered aqueous solution

form

buffered aqueous solution

form

buffered aqueous solution

mol wt

14272 Da

mol wt

14272 Da

mol wt

14688 Da

mol wt

14688 Da

species reactivity

rat, mouse, human

species reactivity

human

species reactivity

human, rat

species reactivity

human, mouse

Physical form

Supplied in PBS with 0.09% (W/V) sodium azide

Disclaimer

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.

Storage Class Code

10 - Combustible liquids

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


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Matteo Bordoni et al.
Cells, 11(8) (2022-04-24)
Mitochondria alterations are present in tissues derived from patients and animal models, but no data are available for peripheral blood mononuclear cells (PBMCs) of ALS patients. This work aims to investigate mitophagy in PBMCs of sporadic (sALS) patients and how
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
Maomao Sun et al.
Frontiers in immunology, 12, 685523-685523 (2021-08-03)
Recent studies have shown that autophagy upregulation can attenuate sepsis-induced acute kidney injury (SAKI). The tumor suppressor p53 has emerged as an autophagy regulator in various forms of acute kidney injury (AKI). Our previous studies showed that p53 acetylation exacerbated
Rongrong Hua et al.
Journal of cellular biochemistry, 120(9), 15915-15923 (2019-05-14)
The sequential reactivation of mechanistic target of rapamycin (mTOR) inhibited autophagic flux in neurons exposed to oxygen-glucose deprivation/reperfusion (OGD/R), which was characterized by reduction of autophagosome formation and restriction of autolysosome degradation. However, its detailed molecular mechanism was still unknown.
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

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