Growth Factor Independence 1b (Gfi1b) is a paralog of Gfi1, sharing nearly identical sequences across their respective protein domains. Gfi1b functions as a transcriptional repressor and is expressed in both the hematopoietic and nervous systems. Its loss of function results in significant defects in hematopoiesis and inner ear development. The two mutant mouse models Gfi1b and P2A are available for licensing and offer unique opportunities for research and therapeutic development.

Gfi1b Knock-In Mouse Model:
This model demonstrates that Gfi1b can effectively substitute for Gfi1 in hematopoiesis, restoring pre-T cell and neutrophil development. Compared to Gfi1 knockouts, these mice exhibit a milder phenotype, enabling in-depth studies of hematopoietic differentiation without severe systemic effects. This model is particularly suited for research focusing on erythroid and megakaryocytic lineages, where Gfi1b is a key regulator.

P2A Point Mutant Mouse Model:
This model highlights the essential role of the SNAG domain in Gfi1’s transcriptional repressor function. The loss of SNAG domain activity replicates the Gfi1 null phenotype, providing a valuable platform for investigating transcriptional regulation and diseases associated with SNAG domain mutations. It is particularly indispensable for studying defects in granulocyte development and inner ear hair cell biology, in particular deafness.

Gfi1 wt GFP and Gfi1b GFP Mouse Models:
There is also a wildtype Gfi1 mouse with a GFP (Green Fluorescence Protein) reporter gene available (Ref. No. 2961) and a Gfi1b mouse with the same GFP reporter gene (Ref. No. 2962).