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Key Documents

PRS3681

Sigma-Aldrich

Anti-ATF6 (ab1) antibody produced in rabbit

affinity isolated antibody, buffered aqueous solution

Synonym(s):

Anti-Activating transcription factor 6

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About This Item

MDL number:
MFCD04040188
UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

species reactivity

human, mouse

technique(s)

immunocytochemistry: suitable
immunofluorescence: suitable
immunohistochemistry: suitable
indirect ELISA: suitable
western blot: suitable

UniProt accession no.

P18850

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... ATF6(22926)

Immunogen

a 16 amino acid peptide from near the carboxy-terminus of human ATF6.

Linkage

The action of this antibody can be blocked using blocking peptide SBP3681.

Physical form

Solution in phosphate buffered saline containing 0.02% 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.

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Description
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Storage Class Code

10 - Combustible liquids

WGK

WGK 2

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Hideaki Tagashira et al.
Biochimica et biophysica acta, 1840(12), 3320-3334 (2014-09-02)
Amyotrophic lateral sclerosis (ALS) is a disease caused by motor neuron degeneration. Recently, a novel SIGMAR1 gene variant (p.E102Q) was discovered in some familial ALS patients. We address mechanisms underlying neurodegeneration caused by the mutation using Neuro2A cells overexpressing σ1R(E102Q)

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