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Merck
CN

SAB4200691

Anti-Insulin antibody, Mouse monoclonal

clone K36AC10, purified from hybridoma cell culture

Synonym(s):

INS

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About This Item

NACRES:
NA.41
UNSPSC Code:
51111800

Key Documents

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Product Name

Anti-Insulin antibody, Mouse monoclonal, clone K36AC10, purified from hybridoma cell culture

biological source

mouse

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

K36AC10, monoclonal

form

buffered aqueous solution

species reactivity

guinea pig, porcine, bovine (proinsulin), rat, monkey, sheep, dog, horse, human (insulin ), rabbit

technique(s)

immunoblotting: suitable
immunocytochemistry: suitable
immunofluorescence: 2.5-5 μg/mL using ß -TC-6 Mouse Embryo Pancrease Insulinoma cells.
immunohistochemistry: 10 μg/mL using heat-retrieved formalin-fixed, paraffin-embedded human pancreas sections and Biotin/ExtrAvidin®-Peroxidase staining system.
radioimmunoassay: suitable

isotype

IgG1

shipped in

dry ice

storage temp.

−20°C

target post-translational modification

unmodified

Quality Level

200

Gene Information

bovine ... Ins(280829)
dog ... Ins(483665)
guinea pig ... Ins(100379579)
horse ... Ins(111776000)
human ... INS(3630)
pig ... Ins(397415)
rabbit ... Ins(100009181)
rhesus monkey ... Ins(704534)

Application

Anti-Insulin antibody, Mouse monoclonal has been used in immunohistochemistry.

Biochem/physiol Actions

Insulin is responsible for two types of actions- excitatory and inhibitory. In its excitatory role, it increases the uptake of glucose and lipid synthesis, and in its inhibitory role it inhibits glycogenolysis, gluconeogenesis, lipolysis, proteolysis and ketogenesis. Aberrant insulin secretion leads to various disorders such as diabetes, hyperglycemia or hypoglycemia. Mutant INS-gene Induced diabetes of youth (MIDY) syndrome is an autosomal dominant disorder caused by missense mutations, which lead to aberrant proinsulin folding. Impaired glucose tolerance (IGT) or non-insulin-dependent diabetes mellitus (NIDDM) is caused by resistance to insulin-stimulated glucose uptake.

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

The INS gene encodes for preproinsulin, which is enzymatically converted into insulin. Insulin is produced by the β cells in the Islets of Langerhans. Preproinsulin is converted to proinsulin in the endoplasmic reticulum and proinsulin is then proteolytically processed to form insulin in newly-forming insulin secretory granules. Insulin production is tightly regulated by specific DNA elements present within ~400 bp in the proximal region of the INS promoter.

Immunogen

Human insulin

Physical form

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

Legal Information

ExtrAvidin is a registered trademark of Merck KGaA, Darmstadt, Germany

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Storage Class

10 - Combustible liquids

wgk

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable

Regulatory Information

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Certificates of Analysis (COA)

Lot/Batch Number
0000419292
0000386018
0000386018
0000419292
0000091423

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Role of insulin resistance in human disease
G M Reaven
Diabetes, 37 (1988)
Cedric S Asensio
Methods in molecular biology (Clifton, N.J.), 2473, 23-28 (2022-07-13)
The retention using selective hook (RUSH) system enables us to synchronize and visualize the movement of cargoes along the secretory pathway. A fluorescently tagged cargo of interest is retained in the endoplasmic reticulum and released in a biotin-dependent manner. Here
Proinsulin misfolding and diabetes: mutant INS gene-induced diabetes of youth
Trends in Endocrinology and Metabolism, 21 (2010)
Covalent histone modifications underlie the developmental regulation of insulin gene transcription in pancreatic beta cells
Swarup K Chakrabarti
The Journal of Biological Chemistry (2003)
Inhibition of Insulin-Degrading Enzyme Does Not Increase Islet Amyloid Deposition in Vitro
Meghan F
Endocrinology (2016)
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