Publications by authors named "R J Garippa"
Article Synopsis
- Ongoing clinical trials highlight the potential of human pluripotent stem cell (hPSC) therapies for treating Parkinson's disease, but a challenge remains in cell death post-transplantation.
- A study used CRISPR-Cas9 screening to discover that p53-induced apoptosis and TNF-α/NF-κB signaling significantly contribute to dopamine neuron death.
- By identifying surface markers for purification and using adalimumab (a TNF-α inhibitor), researchers achieved better survival and integration of dopamine neurons in a mouse model of Parkinson's disease.
Article Synopsis
- Mutations in the SF3B1 gene are prevalent in various cancers and lead to incorrect RNA splicing, but there are currently no treatments to fix these issues.
- Researchers discovered that the protein GPATCH8 is essential for the abnormal splicing caused by mutant SF3B1 and plays a key role in maintaining proper RNA processing.
- By silencing GPATCH8, they found that it corrected many of the splicing errors and improved blood cell formation in models of SF3B1-mutant cancers, suggesting a potential therapeutic approach.
Micronuclei, detected through the cytokinesis-block micronucleus assay, are valuable indicators of ionizing radiation exposure, especially in short-term lymphocyte cultures. The peripheral human blood lymphocyte assay is recognized as a prime candidate for automated biodosimetry. In a prior project at the Columbia University Center for Radiological Research, we automated this assay using the 96-well ANSI/SLAS microplate standard format and relied on established biotech robotic systems named Rapid Automated Biodosimetry Tool (RABiT).
View Article and Find Full Text PDFIncreasing use of covalent and noncovalent inhibitors of Bruton's tyrosine kinase (BTK) has elucidated a series of acquired drug-resistant BTK mutations in patients with B cell malignancies. Here we identify inhibitor resistance mutations in BTK with distinct enzymatic activities, including some that impair BTK enzymatic activity while imparting novel protein-protein interactions that sustain B cell receptor (BCR) signaling. Furthermore, we describe a clinical-stage BTK and IKZF1/3 degrader, NX-2127, that can bind and proteasomally degrade each mutant BTK proteoform, resulting in potent blockade of BCR signaling.
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