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Merck

T7576

Anti-TGN46 antibody produced in rabbit

~1 mg/mL, affinity isolated antibody, buffered aqueous solution

Synonym(s):

Anti-MGC14722, Anti-TGN38 homolog, Anti-TGN48, Anti-TGN51, Anti-TGOLN2, Anti-TTGN2, Anti-Trans-Golgi network integral membrane protein 2 precursor, Anti-Trans-Golgi network protein TGN51, Anti-Trans-golgi network protein 2

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About This Item

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

Product Name

Anti-TGN46 antibody produced in rabbit, ~1 mg/mL, affinity isolated antibody, buffered aqueous solution

biological source

rabbit

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

antigen 80-100 kDa

species reactivity

human

enhanced validation

recombinant expression
Learn more about Antibody Enhanced Validation

concentration

~1 mg/mL

technique(s)

immunoprecipitation (IP): 10-20 μg using TGN46 from human HepG2 cell lysates.
indirect immunofluorescence: 5-10 μg/mL using human A549 cells
western blot (chemiluminescent): 0.25-0.5 μg/mL using extracts of human HEK-293T cells expressing recombinant human TGN46

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Quality Level

Gene Information

human ... TGOLN2(10618)

Application

Rabbit polyclonal anti-TGN46 antibody is used to tag trans-golgi network protein 2 for detection and quantitation by immunocytochemical and immunohistochemical (IHC) techniques such as immunoblotting, immunoprecipitation, and immunofluorescence. It is used as a probe to determine the presence and roles of trans-golgi network protein 2 as a membrane traffic regulating component of the trans-Golgi network (TGN). Anti-TGN46 may be used as a TGN marker.

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.

General description

Anti-TGN46 recognizes human trans-golgi network protein 2 (TGN46). Detection of the TGN46 band by immunoblotting is specifically inhibited by the immunizing peptide.
TGN46 (Trans-Golgi network protein, 46 kDa), the human homologue of rat TGN38, is a resident integral membrane protein of the trans-Golgi network (TGN) that cycles constitutively between the TGN and the plasma membrane, returning via endosomes. The TGN is the major sorting compartment of the secretory pathway for proteins, lipids and membrane traffic. TGN46 is a heavily glycosylated protein, probably involved in regulating membrane traffic to and from the TGN. TGN46 contains a signal peptide, lumenal domain, membrane-spanning domain, and cytoplasmic domain. The membrane spanning region and cytoplasmic tail contain the retention and retrieval signals, respectively for localization in the TGN. TGN46 is widely expressed.

Immunogen

synthetic peptide corresponding to amino acid residues 426-437 of human TGN46 with N-terminal added cysteine, conjugated to KLH. The corresponding sequence is identical in monkey and differs by three amino acids 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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Storage Class

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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Jiehua Li et al.
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Traffic (Copenhagen, Denmark), 11(3), 361-382 (2010-01-15)
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Wolfgang M Schmidt et al.
American journal of human genetics, 97(6), 855-861 (2015-11-20)
Hereditary ataxias comprise a group of genetically heterogeneous disorders characterized by clinically variable cerebellar dysfunction and accompanied by involvement of other organ systems. The molecular underpinnings for many of these diseases are widely unknown. Previously, we discovered the disruption of

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