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SKU:BT-AP10457

IP3R-I(Phospho Ser1764) Polyclonal Antibody

IP3R-I(Phospho Ser1764) Polyclonal Antibody

Regular price $275.00 USD
Regular price Sale price $275.00 USD
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This gene encodes an intracellular receptor for inositol 1,4,5-trisphosphate. Upon stimulation by inositol 1,4,5-trisphosphate, this receptor mediates calcium release from the endoplasmic reticulum. Mutations in this gene cause spinocerebellar ataxia type 15, a disease associated with an heterogeneous group of cerebellar disorders. Multiple transcript variants have been identified for this gene.

The IP3R-I(Phospho Ser1764) Polyclonal Antibody is a highly specific and sensitive tool designed for the detection and analysis of IP3R-I protein phosphorylated at Ser1764. This antibody is produced using advanced immunization techniques and exhibits excellent affinity and selectivity towards the phosphorylated form of IP3R-I.

The IP3R-I protein plays a crucial role in intracellular calcium signaling and is involved in various physiological processes, including cell growth, differentiation, and apoptosis. Phosphorylation of IP3R-I at Ser1764 has been shown to regulate its activity and modulate calcium release from the endoplasmic reticulum.

This polyclonal antibody is rigorously validated for its specificity and sensitivity through various experimental approaches, including Western blotting, immunoprecipitation, and immunofluorescence. It has been extensively tested on a wide range of cell lines and tissues, ensuring reliable and reproducible results.

The IP3R-I(Phospho Ser1764) Polyclonal Antibody is supplied as a ready-to-use solution, eliminating the need for time-consuming and complex antibody preparation procedures. It is provided in a convenient format, allowing for easy storage and handling.

With its exceptional performance and reliability, the IP3R-I(Phospho Ser1764) Polyclonal Antibody is an indispensable tool for researchers studying calcium signaling pathways and investigating the role of IP3R-I phosphorylation in various cellular processes.

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