What is he best known for?
The fields of study he is best known for:
- Enzyme
- Gene
- Organic chemistry
Gregory D. Cuny mainly focuses on Cell biology, Signal transduction, Programmed cell death, Necroptosis and Structure–activity relationship.
His Cell biology research is multidisciplinary, incorporating perspectives in BMPR2, Apoptosis and Spindle apparatus, Spindle checkpoint.
His work on RIPK1 as part of general Programmed cell death research is frequently linked to Jurkat cells, thereby connecting diverse disciplines of science.
While the research belongs to areas of RIPK1, Gregory D. Cuny spends his time largely on the problem of Ripoptosome, intersecting his research to questions surrounding Autophagy, Cell signaling, Kinase and Death domain.
His Necroptosis research includes themes of Necrosis, Pathology and Neuroprotection.
His Structure–activity relationship research is multidisciplinary, relying on both Cell culture, Stereochemistry and Enzyme.
His most cited work include:
- Chemical inhibitor of nonapoptotic cell death with therapeutic potential for ischemic brain injury (1753 citations)
- Identification of RIP1 kinase as a specific cellular target of necrostatins. (1311 citations)
- BMP type I receptor inhibition reduces heterotopic ossification (504 citations)
What are the main themes of his work throughout his whole career to date?
His primary scientific interests are in Biochemistry, Cell biology, Kinase, Organic chemistry and Stereochemistry.
His biological study spans a wide range of topics, including BMPR2 and Small molecule.
His Kinase study incorporates themes from RIPK2 and Phosphorylation.
His studies in Stereochemistry integrate themes in fields like Microsome, Receptor, Chemical synthesis and Alkyl.
His research in Structure–activity relationship intersects with topics in Cell culture and Programmed cell death, Necroptosis.
His work carried out in the field of Programmed cell death brings together such families of science as Ischemia and Pathology.
He most often published in these fields:
- Biochemistry (33.84%)
- Cell biology (16.67%)
- Kinase (14.14%)
What were the highlights of his more recent work (between 2014-2021)?
- Biochemistry (33.84%)
- Cell biology (16.67%)
- Enzyme (8.08%)
In recent papers he was focusing on the following fields of study:
Gregory D. Cuny spends much of his time researching Biochemistry, Cell biology, Enzyme, Kinase and Spinal muscular atrophy.
In his work, Nucleotide salvage, Purine nucleotide salvage and Purine is strongly intertwined with Cryptosporidium parvum, which is a subfield of Biochemistry.
His Cell biology study frequently links to adjacent areas such as Small molecule.
Gregory D. Cuny has researched Enzyme in several fields, including Francisella tularensis and Antibacterial activity.
Gregory D. Cuny combines subjects such as RIPK2 and ADME with his study of Kinase.
His Cancer research research focuses on Allosteric regulation and how it connects with Signal transduction.
Between 2014 and 2021, his most popular works were:
- Structure Guided Design of Potent and Selective Ponatinib-Based Hybrid Inhibitors for RIPK1 (86 citations)
- Restored glial glutamate transporter EAAT2 function as a potential therapeutic approach for Alzheimer’s disease (66 citations)
- Restored glial glutamate transporter EAAT2 function as a potential therapeutic approach for Alzheimer’s disease (66 citations)
In his most recent research, the most cited papers focused on:
- Enzyme
- Gene
- Organic chemistry
Gregory D. Cuny mainly investigates Biochemistry, Enzyme, Inosine, Dehydrogenase and Mycobacterium tuberculosis.
He regularly ties together related areas like Cryptosporidium parvum in his Biochemistry studies.
Gregory D. Cuny has included themes like IMP dehydrogenase and Xanthosine in his Enzyme study.
His Inosine research incorporates elements of Benzoxazole, Biosynthesis and Guanine salvage, Guanine, Inosine-5′-monophosphate dehydrogenase.
This overview was generated by a machine learning system which analysed the scientist’s
body of work. If you have any feedback, you can
contact us
here.
