41 results on '"Young, Samuel N."'
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2. Phosphorylation-dependent pseudokinase domain dimerization drives full-length MLKL oligomerization
3. A common human MLKL polymorphism confers resistance to negative regulation by phosphorylation
4. Inhibitors identify an auxiliary role for mTOR signalling in necroptosis execution downstream of MLKL activation.
5. Co-clustering of EphB6 and ephrinB1 in trans restrains cancer cell invasion
6. Identification of MLKL membrane translocation as a checkpoint in necroptotic cell death using Monobodies
7. Human RIPK3 C-lobe phosphorylation is essential for necroptotic signaling
8. A toolbox for imaging RIPK1, RIPK3, and MLKL in mouse and human cells
9. Ubiquitylation of MLKL at lysine 219 positively regulates necroptosis-induced tissue injury and pathogen clearance
10. Conformational interconversion of MLKL and disengagement from RIPK3 precede cell death by necroptosis
11. Granulovirus PK-1 kinase activity relies on a side-to-side dimerization mode centered on the regulatory αC helix
12. Human RIPK3 maintains MLKL in an inactive conformation prior to cell death by necroptosis
13. A robust methodology to subclassify pseudokinases based on their nucleotide-binding properties.
14. It takes two to tango: structure of viral kinase PK-1 reveals a new mode of kinase regulation
15. A family harboring an MLKL loss of function variant implicates impaired necroptosis in diabetes
16. MLKL trafficking and accumulation at the plasma membrane control the kinetics and threshold for necroptosis
17. A missense mutation in the MLKL brace region promotes lethal neonatal inflammation and hematopoietic dysfunction
18. Distinct pseudokinase domain conformations underlie divergent activation mechanisms among vertebrate MLKL orthologues
19. The brace helices of MLKL mediate interdomain communication and oligomerisation to regulate cell death by necroptosis
20. A common humanMLKLpolymorphism confers resistance to negative regulation by phosphorylation
21. Activation of the pseudokinase MLKL unleashes the four-helix bundle domain to induce membrane localization and necroptotic cell death
22. Oligomerization‐driven MLKL ubiquitylation antagonizes necroptosis
23. The intracellular domains of the EphB6 and EphA10 receptor tyrosine pseudokinases function as dynamic signalling hubs
24. SMCHD1's ubiquitin-like domain is required for N-terminal dimerization and chromatin localization
25. A missense mutation in the MLKL brace region promotes lethal neonatal inflammation and hematopoietic dysfunction.
26. The Pseudokinase MLKL Mediates Necroptosis via a Molecular Switch Mechanism
27. Suppression of Cytokine Signaling by SOCS3: Characterization of the Mode of Inhibition and the Basis of Its Specificity
28. A toolbox for imaging RIPK1, RIPK3 and MLKL in mouse and human cells
29. Viral MLKL Homologs Subvert Necroptotic Cell Death by Sequestering Cellular RIPK3
30. Missense mutations in the MLKL ‘brace’ region lead to lethal neonatal inflammation in mice and are present in high frequency in humans
31. Crystal structure of the hinge domain of Smchd1 reveals its dimerization mode and nucleic acid–binding residues.
32. Conformational switching of the pseudokinase domain promotes human MLKL tetramerization and cell death by necroptosis
33. The epigenetic regulator Smchd1 contains a functional GHKL-type ATPase domain
34. Necroptosis signalling is tuned by phosphorylation of MLKL residues outside the pseudokinase domain activation loop
35. Mechanistic insights into activation and SOCS3-mediated inhibition of myeloproliferative neoplasm-associated JAK2 mutants from biochemical and structural analyses
36. Functional characterization of c-Mpl ectodomain mutations that underlie congenital amegakaryocytic thrombocytopenia
37. Insights into the evolution of divergent nucleotide-binding mechanisms among pseudokinases revealed by crystal structures of human and mouse MLKL
38. A robust methodology to subclassify pseudokinases based on their nucleotide-binding properties
39. The epigenetic regulator Smchd1 contains a functional GHKL-type ATPase domain.
40. Large-scale genomic investigation of pediatric cholestasis reveals a novel hepatorenal ciliopathy caused by PSKH1 mutations.
41. The VEGFR/PDGFR tyrosine kinase inhibitor, ABT-869, blocks necroptosis by targeting RIPK1 kinase.
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