The switch from fetal γ-globin to adult β-globin is controlled by BCL11A. Genetic manipulation of BCL11A improves disease outcomes by turning γ-globin expression back on to compensate for ...

Destabilizing BCL11A In the new work, Orkin and his colleagues explored the structure and chemistry of the BCL11A protein, looking for ways to hit it.

For example, Bcl11a deficiency contributes to both the abnormal generation of natural killer-like cells in the thymus and the underdevelopment of the cortex, whereas outright loss of Bcl11b does not.

BCL11A: Evidence for neuroprotective effect Date: September 14, 2021 Source: University of Bonn Summary: The neurotransmitter dopamine influences the activity of a wide variety of brain areas. A ...

The team used human cells and a mouse model to show that the body needs two healthy copies of BCL11A to make enough of the BCL11A protein for brain cells to develop normally and work at capacity.

A self-inactivating lentivirus vector with a short hairpin RNA designed to interfere with BCL11A expression was inserted into autologous hematopoietic stem cells of patients with sickle cell ...

In a form of sickle cell disease called sickle cell anemia, mutations in a gene called HBB affect the protein’s structure, causing it to twist normally round red blood cells into a curved sickle ...

BCL11A: Evidence for neuroprotective effect Researchers at the University of Bonn investigate the role of the transcription factor for dopamine-producing neurons Peer-Reviewed Publication ...

Based on these and other observations, the researchers identified a distinctive disease mechanism in which mutant BCL11B binds to BCL11A and manages to interfere with the normal function of that ...