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Zika Virus Disrupts Neural Progenitor Development and Leads to Microcephaly in Mice.
TLDR
This model provides evidence for a direct link between Zika virus infection and microcephaly, with potential for further exploration of the underlying mechanisms and management of ZIKV-related pathological effects during brain development.
Zika Virus Disrupts Neural Progenitor Development and Leads to Microcephaly in Mice.
TLDR
The dataset has now been submitted to the Genome Sequence Archive of the Beijing Institute of Genomics Data Center under the accession number PRJCA000267 and the online version of the paper has been modified to include an Accession Numbers section.
The MLK Family Mediates c-Jun N-Terminal Kinase Activation in Neuronal Apoptosis
TLDR
It is shown that members of the mixed-lineage kinase (MLK) family are expressed in neuronal cells and are likely to act between Rac1/Cdc42 and MKK4 and -7 in death signaling, and findings place the MLKs upstream of mitochondrial cytochromec release and caspase activation.
POSH acts as a scaffold for a multiprotein complex that mediates JNK activation in apoptosis
TLDR
POSH appears to function as a scaffold in a multiprotein complex that links activated Rac1 and downstream elements of the JNK apoptotic cascade, which is required for neuronal death induced by various means including nerve growth factor deprivation.
β‐Amyloid‐induced neuronal apoptosis requires c‐Jun N‐terminal kinase activation
TLDR
The observations implicate the JNK pathway as a required element in death evoked by Aβ and hence identify it as a potential therapeutic target in AD.
CEP-1347 (KT7515), a Semisynthetic Inhibitor of the Mixed Lineage Kinase Family*
TLDR
Results identify MLKs as targets of CEP-1347 in the JNK signaling cascade and demonstrate that CEP -1347 can block MLK-induced cell death.
Leucine‐rich repeat kinase 2 disturbs mitochondrial dynamics via Dynamin‐like protein
J. Neurochem. (2012) 122, 650–658.
Direct Interaction of the Molecular Scaffolds POSH and JIP Is Required for Apoptotic Activation of JNKs*
TLDR
It is reported that propagation of the apoptotic JNK pathway requires the cooperative interaction of two molecular scaffolds, POSH and JIPs, and that PJAC (POSH-JIP apoptotic complex), that includes all of the known kinase components of the pathway.
β‐Amyloid‐induced neuronal apoptosis requires c‐Jun N‐terminal kinase activation
TLDR
The observations implicate the JNK pathway as a required element in death evoked by Aβ and hence identify it as a potential therapeutic target in AD.
Siah1 Interacts with the Scaffold Protein POSH to Promote JNK Activation and Apoptosis*
TLDR
A “loop” mechanism in which the JNK pathway promotes SIAH1 stabilization and in which SIAh1 in turn activates the J NK pathway and, ultimately, contributes to cell death is revealed.
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