|Reactivity||Human, Mouse, Rat, Hamster, Bovine|
|Calculated MW||28232 Da|
|Application & Usage||Western blotting (0.5-4 µg/ml). However, the optimal concentrations should be determined individually. The antibody recognizes ~30 kDa InSig-1 and its precursor (~50 kDa) in samples from human, mouse and rat origins. Reactivity to other species has not been tested.|
|Other Names||CL-6 , INSIG1 , MGC1405|
|Formulation||100 µg (0.5 mg/ml) affinity purified rabbit polyclonal antibody in phosphate-buffered saline (PBS) containing 30% glycerol, 0.5% BSA, and 0.01% thimerosal.|
|Handling||The antibody solution should be gently mixed before use.|
|Reconstitution & Storage||-20 °C|
|Precautions||Insig1 Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Mediates feedback control of cholesterol synthesis by controlling SCAP and HMGCR. Functions by blocking the processing of sterol regulatory element-binding proteins (SREBPs). Capable of retaining the SCAP-SREBF2 complex in the ER thus preventing it from escorting SREBPs to the Golgi. Initiates the sterol-mediated ubiquitin-mediated endoplasmic reticulum-associated degradation (ERAD) of HMGCR via recruitment of the reductase to the ubiquitin ligase, AMFR/gp78. May play a role in growth and differentiation of tissues involved in metabolic control. May play a regulatory role during G0/G1 transition of cell growth (By similarity).|
|Cellular Location||Endoplasmic reticulum membrane; Multi-pass membrane protein|
|Tissue Location||Highly expressed in liver and kidney.|
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Provided below are standard protocols that you may find useful for product applications.
Insulin-induced gene (InSig) localizes in the endoplasmic recticulum(ER) and is highly expressed in the liver and fibroblast cell lines. InSig1 and InSig2 play important roles in the regulation of cholesterol biosynthesis. Sterol induces InSig1 binding to the sterol-sensing domain of SREBP cleavage-activating protein (SCAP). Both InSig1 and Insig2 prevent the export of SCAP from the ER and thus, inhibit cholesterol synthesis by preventing the proteolytic cleavage of SREBPs by the Golgi enzymes.
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