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SAB4200691

Sigma-Aldrich

Anti-Insulin antibody, Mouse monoclonal

clone K36AC10, purified from hybridoma cell culture

Sinônimo(s):

INS

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About This Item

Código UNSPSC:
51111800
NACRES:
NA.41

fonte biológica

mouse

Nível de qualidade

forma do anticorpo

purified immunoglobulin

tipo de produto de anticorpo

primary antibodies

clone

K36AC10, monoclonal

forma

buffered aqueous solution

reatividade de espécies

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

técnica(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

Isotipo

IgG1

Condições de expedição

dry ice

temperatura de armazenamento

−20°C

modificação pós-traducional do alvo

unmodified

Informações sobre genes

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)

Descrição geral

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.

Imunogênio

Human insulin

Aplicação

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

Ações bioquímicas/fisiológicas

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.

forma física

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

Informações legais

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

Exoneração de responsabilidade

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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Código de classe de armazenamento

10 - Combustible liquids

Classe de risco de água (WGK)

WGK 1

Ponto de fulgor (°F)

Not applicable

Ponto de fulgor (°C)

Not applicable


Certificados de análise (COA)

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Visite a Biblioteca de Documentos

Inhibition of Insulin-Degrading Enzyme Does Not Increase Islet Amyloid Deposition in Vitro
Meghan F
Endocrinology (2016)
Covalent histone modifications underlie the developmental regulation of insulin gene transcription in pancreatic beta cells
Swarup K Chakrabarti
The Journal of Biological Chemistry (2003)
Proinsulin misfolding and diabetes: mutant INS gene-induced diabetes of youth
Trends in Endocrinology and Metabolism, 21 (2010)
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
Recessive mutations in the INS gene result in neonatal diabetes through reduced insulin biosynthesis
Intza Garin
Proceedings of the National Academy of Sciences of the USA, 107 (2010)

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