Out-licensing

Development of G2A GPCR Deficient Mouse Model and G2A Monoclonal Antibody

Introduction/Background

G2A, initially an orphan GPCR, was identified in a search for downstream transcriptional targets of the oncogene BCR-ABL tyrosine kinase. G2A belongs to a family of sequence related GPCRs that were initially thought to bind to proinflammatory lipids. However it was recently discovered that G2A and its related GPCRs act as proton sensors that increase the acid-induced production of secondary messengers such as inositol phosphates and cyclic AMP.

G2A is expressed mainly in immune cells including T and B-lymphocytes, monocytes, macrophages and dendritic cells. Currently, G2A and its related GPCRs are implicated in a variety of diseases including autoimmune disorders, inflammation and cancer. However the exact biological functions of these GPCRs have not been elucidated.

Aims/Hypothesis

Therefore, readily available research tools could significantly accelerate the research to better understand the role of these GPCRs under physiological and pathological conditions.

Research

Researchers at UCLA identified, characterized and patented the G2A GPCR. To help in the elucidation of the biological functions of G2A, these researchers have also developed a G2A GPCR deficient mouse model along with polyclonal and monoclonal antibodies useful for immunoprecipitations and Western blots. These tools may be used to study G2A to better understand its function in a variety of disorders and to also develop therapeutics that target this GPCR.

Conclusion

We have developed a readily available G2A deficient mouse model that can be used to study G2A and used as a screen for novel therapies that involve G2A dysfunction and readily available G2A antibodies may be used for immunoprecipitations and Western blots to screen for G2A expression.

Relevance/Opportunity

Please enquire regarding licensing opportunities quoting reference no. 1997-538.

Preclinical

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