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SAB4200074

Sigma-Aldrich

Anti-VAC14 antibody produced in rabbit

~1.5 mg/mL, affinity isolated antibody, buffered aqueous solution

Synonym(s):

Anti-ArPIKfyve, Anti-TAX1-binding protein 2, Anti-TAX1BP2, Anti-TAX1BP2 TAX-reactive protein x, Anti-TRX

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About This Item

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

mol wt

antigen ~82 kDa

species reactivity

human

packaging

antibody small pack of 25 μL

concentration

~1.5 mg/mL

technique(s)

immunoprecipitation (IP): 10-15 μg using A431 cell lysates
indirect immunofluorescence: 8-16 μg/mL using HeLa cells
western blot: 1.5-3.0 μg/mL using HeLa cell lysates

UniProt accession no.

Q08AM6

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... VAC14(55697)

General description

VAC14 (VAC14 component of PIKFYVE complex) gene (also known as ArPIKfyve, TAX1BP2, TRX) is mapped within human chromosome 16q22.1-q22.2 and encodes a scaffold protein. This protein is a component of phosphoinositide kinase, FYVE-type zinc finger containing (PIKfyve) protein kinase complex.

Application

Anti-VAC14 antibody produced in rabbit has been used in:
  • immunoblotting
  • immunoprecipitation
  • immunofluorescence

Biochem/physiol Actions

VAC14 is a regulator of phosphoinositide kinase, FYVE-type zinc finger containing (PIP5K3/PIKfyve), a dual specificity kinase that phosphorylates phosphatidylinositol 3-phosphate (PtdIns3P). This generates housekeeping phospholipid PtdIns(3,5)P2, that controls multivesicular body morphology, retrograde traffic to the trans-Golgi network and is critical for neuronal survival. VAC14/ArPIKfyve upregulates PIKfyve phosphoinositide-5-kinase activity. In 3T3-L1 adipocytes, VAC14 and PIP5K3 interaction has been shown to play a critical role in insulin-regulated glucose transporter (GLUT4) translocation from intracellular storage compartment to the cell surface. Knockout of the VAC14 gene in mouse results in massive neurodegeneration and affects neurons in the midbrain and of the peripheral sensory system.

Physical form

Solution in 0.01 M phos­phate buffered saline, pH 7.4, containing 15 mM 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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Storage Class Code

10 - Combustible liquids

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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Monica I Alvarez et al.
Proceedings of the National Academy of Sciences of the United States of America, 114(37), E7746-E7755 (2017-08-23)
Risk, severity, and outcome of infection depend on the interplay of pathogen virulence and host susceptibility. Systematic identification of genetic susceptibility to infection is being undertaken through genome-wide association studies, but how to expeditiously move from genetic differences to functional
Human genetic variation in VAC14 regulates Salmonella invasion and typhoid fever through modulation of cholesterol
Alvarez M, et al.
Proceedings of the National Academy of Sciences of the USA, 114(37), E7746-E7755 (2017)
Loss of Vac14, a regulator of the signaling lipid phosphatidylinositol 3, 5-bisphosphate, results in neurodegeneration in mice
Zhang Y, et al.
Proceedings of the National Academy of Sciences of the USA, 104(44), 17518-17523 (2007)
VAC14 nucleates a protein complex essential for the acute interconversion of PI3P and PI (3, 5) P2 in yeast and mouse
Jin N, et al.
The Embo Journal, 27(24), 3221-3234 (2008)
Seong M Kim et al.
The Journal of clinical investigation, 126(11), 4088-4102 (2016-11-02)
Oncogenic mutations drive anabolic metabolism, creating a dependency on nutrient influx through transporters, receptors, and macropinocytosis. While sphingolipids suppress tumor growth by downregulating nutrient transporters, macropinocytosis and autophagy still provide cancer cells with fuel. Therapeutics that simultaneously disrupt these parallel
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