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A1486

Sigma-Aldrich

Anti-ATP6AP1 (451-465) antibody produced in rabbit

IgG fraction of antiserum, PBS solution

Synonyme(s) :

Anti-16A, Anti-ATP6IP1, Anti-ATP6S1, Anti-Ac45, Anti-CF2, Anti-VATPS1, Anti-Vacuolar ATP synthase subunit S1 precursor, Anti-XAP3

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About This Item

Code UNSPSC :
12352203
Nomenclature NACRES :
NA.41

Source biologique

rabbit

Niveau de qualité

200

Conjugué

unconjugated

Forme d'anticorps

IgG fraction of antiserum

Type de produit anticorps

primary antibodies

Clone

polyclonal

Forme

PBS solution

Poids mol.

antigen ~52 kDa

Espèces réactives

human

Technique(s)

western blot: 1:500-1:2,000

Numéro d'accès UniProt

Q15904

Conditions d'expédition

dry ice

Température de stockage

−20°C

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

human ... ATP6AP1(537)

Description générale

ATPase H+ transporting accessory protein 1 (ATP6AP1) is an accessory subunit of the V-ATPase. This gene is located on human chromosome Xq28. ATP6AP1 is also referred as Ac45. It is abundantly expressed a high levels in neuronal and (neuro-) endocrine cells and osteoclasts.

Immunogène

synthetic peptide corresponding to amino acids 451-465 of human ATP6AP1

Application

Rabbit anti-ATP6AP1 (451-465) antibody can be used for western blot (1:500-1:2,000) assays.
Yale Center for High Throughput Cell Biology IF-tested antibodies. Each antibody is tested by immunofluorescence against HUVEC cells using the Yale HTCB IF protocol. To learn more about us and Yale Center for High Throughput Cell Biology partnership, visit sigma.com/htcb-if.

Actions biochimiques/physiologiques

ATPase H+ transporting accessory protein 1 (ATP6AP1) is known to cause an X-linked N-glycosylation syndrome with liver disease. It is essential for endosomal acidification. It also participates in membrane trafficking and Ca2+-dependent membrane fusion.

Forme physique

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

Clause de non-responsabilité

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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Code de la classe de stockage

12 - Non Combustible Liquids

Classe de danger pour l'eau (WGK)

nwg

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable

Certificats d'analyse (COA)

Recherchez un Certificats d'analyse (COA) en saisissant le numéro de lot du produit. Les numéros de lot figurent sur l'étiquette du produit après les mots "Lot" ou "Batch".

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Consulter la Bibliothèque de documents

Expanding the phenotype of metabolic cutis laxa with an additional disorder of N-linked protein glycosylation
Witters P, et al.
European Journal of Human Genetics, 26(5), 618-618 (2018)
Loss-of-function mutations in ATP6AP1 and ATP6AP2 in granular cell tumors
Pareja F, et al.
Nature Communications, 9(1), 3533-3533 (2018)
Richard J Nuckels et al.
Investigative ophthalmology & visual science, 50(2), 893-905 (2008-10-07)
The vacuolar (v)-ATPase complex is a key regulator of the acidification of endosomes, lysosomes, and the luminal compartments of several cell types, tissues, and organs; however, little is know about the in vivo function of the v-ATPase complex or its
Jason J Gokey et al.
Developmental biology, 407(1), 115-130 (2015-08-09)
Asymmetric fluid flows generated by motile cilia in a transient 'organ of asymmetry' are involved in establishing the left-right (LR) body axis during embryonic development. The vacuolar-type H(+)-ATPase (V-ATPase) proton pump has been identified as an early factor in the
Fresia Pareja et al.
Nature communications, 9(1), 3533-3533 (2018-09-01)
Granular cell tumors (GCTs) are rare tumors that can arise in multiple anatomical locations, and are characterized by abundant intracytoplasmic granules. The genetic drivers of GCTs are currently unknown. Here, we apply whole-exome sequencing and targeted sequencing analysis to reveal
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