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Merck

SAB4200691

Sigma-Aldrich

Anti-Insulin antibody, Mouse monoclonal

clone K36AC10, purified from hybridoma cell culture

Synonym(e):

INS

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About This Item

UNSPSC-Code:
51111800
NACRES:
NA.41

Biologische Quelle

mouse

Qualitätsniveau

Antikörperform

purified immunoglobulin

Antikörper-Produkttyp

primary antibodies

Klon

K36AC10, monoclonal

Form

buffered aqueous solution

Speziesreaktivität

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

Methode(n)

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

Isotyp

IgG1

Versandbedingung

dry ice

Lagertemp.

−20°C

Posttranslationale Modifikation Target

unmodified

Angaben zum Gen

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)

Allgemeine Beschreibung

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

Anwendung

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

Biochem./physiol. Wirkung

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.

Physikalische Form

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

Rechtliche Hinweise

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

Haftungsausschluss

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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Lagerklassenschlüssel

10 - Combustible liquids

WGK

WGK 1

Flammpunkt (°F)

Not applicable

Flammpunkt (°C)

Not applicable


Analysenzertifikate (COA)

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In der Dokumentenbibliothek finden Sie die Dokumentation zu den Produkten, die Sie kürzlich erworben haben.

Die Dokumentenbibliothek aufrufen

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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