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SAB4200427

Sigma-Aldrich

Anti-COG8 (C-terminal) antibody produced in rabbit

~1.0 mg/mL, affinity isolated antibody

Synonym(s):

Anti-CDG2H, Anti-COG complex subunit 8, Anti-Component of oligomeric golgi complex 8, Anti-conserved oligomeric Golgi complex subunit 8, Anti-conserved oligomeric golgi complex component 8, Anti-dependent on RIC1, AntiDOR1

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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 ~70 kDa

species reactivity

human

concentration

~1.0 mg/mL

technique(s)

immunoprecipitation (IP): 5-10 μg using lysates of human HEK-293T cells
indirect immunofluorescence: 0.5-1.0 μg/mL using using human HeLa cells
western blot: 1-2 μg/mL using whole extracts of human HEK-293 cells

UniProt accession no.

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... COG8(84342)

General description

Conserved oligomeric Golgi complex 8 (COG8), also known as DOR1 or CDG2H, is a member of the conserved oligomeric Golgi (COG) complex. COG complex is composed of eight distinct subunits organized as heterotrimeric groups namely Cog2-Cog3-Cog4 and Cog5-Cog6-Cog7. They are interlinked by the dimeric group comprising Cog1 and Cog8.

Specificity

Anti-COG8 (C-terminal) recognizes human COG8.

Immunogen

synthetic peptide corresponding to the C-terminal region of human COG8, conjugated to KLH

Application

Anti-COG8 (C-terminal) antibody produced in rabbit may be used in:
  • immunoblotting
  • immunoprecipitation
  • immunofluorescence

Biochem/physiol Actions

COG complex, is an evolutionarily conserved multi-subunit protein complex that regulates membrane trafficking and maintenance of Golgi glycosylation machinery in eukaryotic cells. Mutations in the COG8 gene cause congenital disorder of glycosylation, type IIh, a disease that is characterized by under-glycosylated serum proteins, and whose symptoms include severe psychomotor retardation, failure to thrive, seizures, and dairy and wheat product intolerance.

Physical form

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

Storage and Stability

For continuous use, store at 2-8 °C for up to one month. For extended storage freeze in working aliquots. Repeated freezing and thawing is not recommended. If slight turbidity occurs upon prolonged storage, clarify the solution by centrifugation before use. Working dilution samples should be discarded if not used within 12 hours.

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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COG8 deficiency causes new congenital disorder of glycosylation type IIh
Kranz C, et al.
Human Molecular Genetics, 16(7), 731-741 (2007)
Modeling congenital disorders of N-linked glycoprotein glycosylation in Drosophila melanogaster
Frappaolo A, et al.
Frontiers in Genetics, 9, 436-436 (2018)
Role of the conserved oligomeric Golgi (COG) complex in protein glycosylation
Smith RD and Lupashin VV
Carbohydrate Research, 343(12), 2024-2031 (2008)
Farhana Taher Sumya et al.
Traffic (Copenhagen, Denmark), 24(2), 52-75 (2022-12-06)
Conserved Oligomeric Golgi (COG) complex controls Golgi trafficking and glycosylation, but the precise COG mechanism is unknown. The auxin-inducible acute degradation system was employed to investigate initial defects resulting from COG dysfunction. We found that acute COG inactivation caused a
Comparative analyses of the Conserved Oligomeric Golgi (COG) complex in vertebrates
Quental R, et al.
BMC Evolutionary Biology, 10(1), 212-212 (2010)

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