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Merck

A0856

Anti-ATG5 (N-terminal) antibody produced in rabbit

affinity isolated antibody, PBS solution

Synonyme(s) :

Anti-APG5, Anti-APG5L, Anti-ASP, Anti-ATG5 autophagy related 5 homolog (S. cerevisiae), Anti-Apoptosis-specific protein, Anti-Autophagy protein 5-like

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A propos de cet article

UNSPSC Code:
12352203
NACRES:
NA.41
MDL number:
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Nom du produit

Anti-ATG5 (N-terminal) antibody produced in rabbit, affinity isolated antibody, PBS solution

biological source

rabbit

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

PBS solution

mol wt

antigen ~56 kDa (Atg5-Atg12 complex)

species reactivity

mouse, human, rat

packaging

antibody small pack of 25 μL

technique(s)

immunofluorescence: suitable
western blot: 0.5-1 μg/mL using whole extracts of human K562, rat NRK, and mouse 3T3 cells

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Quality Level

Gene Information

human ... ATG5(9474)
mouse ... Atg5(11793)
rat ... Atg5(365601)

Application

Anti-ATG5 (N-terminal) antibody has been used:
  • in immunoblotting
  • in immunofluorescence
  • in western blotting

Applications in which this antibody has been used successfully, and the associated peer-reviewed papers, are given below.
Western Blotting (1 paper)
Rabbit anti-ATG5 (N-terminal specific) was used for western blot analysis to detect the level of ATG5 in SK-N-MC cells after transduction with an adenovirus expressing a shRNA specific to ATG5.
Rabbit anti-ATG5 has been used for immunofluorescence and chemiluminescent western blot analyses.

Biochem/physiol Actions

Atg5 (Apg5) is a 32 kDa protein that is required for autophagy. Atg5 is covalently modified by Atg12, a ubiquitin-like modifier. The Atg12-Atg5-Atg16 complex thus formed, localizes to autophagosome precursors and regulates autophagosome formation. Studies have reported that Atg5 fragment that is formed by calpain cleavage has pro-apoptotic properties.
Rabbit anti-ATG5 (N-terminal) recognizes human, rat, and mouse Atg5-Atg12 complex.

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.

Immunogen

synthetic peptide corresponding to amino acids 2-15 of human ATG5, conjugated to KLH via a C-terminal cysteine residue. The corresponding sequence is identical in rat and mouse.

Physical form

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

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Classe de stockage

10 - Combustible liquids

wgk

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

ppe

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


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Consulter la Bibliothèque de documents

Defective autophagy in vascular smooth muscle cells accelerates senescence and promotes neointima formation and atherogenesis
Grootaert M O A J, et al.
Autophagy, 11(11), 2014-2032 (2015)
Soraya Santana et al.
Neurobiology of aging, 33(2), 430-430 (2011-01-29)
Mounting evidence suggests that herpes simplex virus type 1 (HSV-1) is involved in the pathogenesis of Alzheimer's disease (AD). Epidemiological analyses have shown that HSV-1 is a risk factor for AD in people with at least 1 type 4 allele
Autophagy adaptor protein p62/SQSTM1 and autophagy-related gene Atg5 mediate autophagosome formation in response to Mycobacterium tuberculosis infection in dendritic cells
Seto S, et al.
PLoS ONE, 8(12), e86017-e86017 (2013)
Denitsa S Petkova et al.
Viruses, 9(5) (2017-05-23)
Autophagy is a potent cell autonomous defense mechanism that engages the lysosomal pathway to fight intracellular pathogens. Several autophagy receptors can recognize invading pathogens in order to target them towards autophagy for their degradation after the fusion of pathogen-containing autophagosomes
Shintaro Seto et al.
PloS one, 8(12), e86017-e86017 (2014-01-01)
Mycobacterium tuberculosis is an intracellular pathogen that can survive within phagocytic cells by inhibiting phagolysosome biogenesis. However, host cells can control the intracellular M. tuberculosis burden by the induction of autophagy. The mechanism of autophagosome formation to M. tuberculosis has

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