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C1743

Sigma-Aldrich

Anti-Cul7 antibody, Mouse monoclonal

clone Ab38, purified from hybridoma cell culture

Synonyma:

Anti-Cullin 7, Anti-KIAA007

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About This Item

MDL number:
MFCD09265422
UNSPSC Code:
12352203
NACRES:
NA.41

biological source

mouse

Quality Level

200

conjugate

unconjugated

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

Ab38, monoclonal

form

buffered aqueous solution

mol wt

antigen ~180 kDa

species reactivity

human, mouse

concentration

~2 mg/mL

technique(s)

immunoprecipitation (IP): suitable
western blot: 0.5-1 μg/mL using 3T3 total cel extract

isotype

IgG2b

UniProt accession no.

Q14999

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... CUL7(9820)
mouse ... Cul7(66515)

General description

Monoclonal Anti-Cul7 (mouse IgG2b isotype) is derived from the hybridoma Ab38 produced by the fusion of mouse myeloma cells (P3X63Ag8.653) and splenocytes from BALB/c mice immunized with mouse Cul7. CUL7 is expressed in all tissues and cell lines except testis and small intestine.

Immunogen

mouse Cul7.

Application

Monoclonal Anti-Cul7 antibody produced in mouse is suitable for immunoprecipitation and western blotting at a concentration of 0.5-1μg/mL using 3T3 total cel extract.

Biochem/physiol Actions

CUL7 functions to promote cell growth through and antagonizes the function of p53.
Cullin-7 (cul7) is a protein encoded by the CUL7 gene in humans. It is also referred as 3M1, KIAA0076 and dJ20C7.5. Mutation in CUL7 gene is majorly responsible for 3M syndrome (is a rare autosomal recessive disorder). CUL7 acts as a novel gene potentially involved in liver carcinogenesis associated with metabolic syndrome (MS) and its amplification may influence cell proliferation.

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

10 - Combustible liquids

wgk_germany

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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Osvědčení o analýze (COA)

Lot/Batch Number
079M4824V
127M4759V
104M4821V
017K4768

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Cytoplasmic localized ubiquitin ligase cullin 7 binds to p53 and promotes cell growth by antagonizing p53 function
Andrews P, et al.
Oncogene, 25(33), 4534-4534 (2006)
Céline Huber et al.
Best practice & research. Clinical endocrinology & metabolism, 25(1), 143-151 (2011-03-15)
3M syndrome (MIM 273750) is an autosomal recessive disorder characterized by pre- and post-natal growth retardation (<-4 SD), facial dysmorphism, large head circumference, normal intelligence and endocrine function. Skeletal changes include long slender tubular bones and tall vertebral bodies. There
Céline Huber et al.
European journal of human genetics : EJHG, 17(3), 395-400 (2009-02-20)
The 3M syndrome is a rare autosomal recessive disorder recently ascribed to mutations in the CUL7 gene and characterized by severe pre- and postnatal growth retardation. Studying a series of 33 novel cases of 3M syndrome, we have identified deleterious
Valerie Paradis et al.
Gut, 62(6), 911-919 (2012-09-04)
Metabolic syndrome (MS) is an emerging risk factor in hepatocellular carcinoma (HCC). HCC related to MS may occur either in advanced fibrosis or before the development of cirrhosis, suggesting involvement of different molecular pathways according to the features of background
Cristina Meazza et al.
Italian journal of pediatrics, 39, 21-21 (2013-03-23)
3-M syndrome is a rare autosomal recessive disorder that causes short stature, unusual facial features and skeletal abnormalities. Mutations in the CUL7, OBSL1 and CCDC8 genes could be responsible for 3-M syndrome.Here we describe the growth and evolution of dismorphic
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