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Neurotoxins affecting neuroexocytosis.
TLDR
The mechanism of action of three groups of presynaptic neurotoxins that interfere directly with the process of neurotransmitter release is reviewed, whereas presynapses acting on ion channels are not dealt with here. Expand
Tetanus and botulinum-B neurotoxins block neurotransmitter release by proteolytic cleavage of synaptobrevin
TLDR
The results indicate that tetanus and botulinum B neurotoxins block neurotransmitter release by cleaving synaptobrevin-2, a protein that, on the basis of the results, seems to play a key part in neurotransmitterRelease. Expand
Mutations in Dynein Link Motor Neuron Degeneration to Defects in Retrograde Transport
TLDR
It is shown that missense point mutations in the cytoplasmic dynein heavy chain result in progressive motor neuron degeneration in heterozygous mice, and in homozygotes this is accompanied by the formation of Lewy-like inclusion bodies, thus resembling key features of human pathology. Expand
Rab5 and Rab7 Control Endocytic Sorting along the Axonal Retrograde Transport Pathway
TLDR
The data demonstrate that TeNT H(C) uses a retrograde transport pathway shared with p75(NTR), TrkB, and BDNF, which is strictly dependent on the activities of both Rab5 and Rab7, and therefore Rab7 plays an essential role in axonal retrogrades transport by controlling a vesicular compartment implicated in neurotrophin traffic. Expand
Immunocytochemical techniques reveal multiple, distinct cellular pools of PtdIns4P and PtdIns(4,5)P2
TLDR
Specific conditions that enable preservation of several organellar membranes for the immunocytochemical detection of PtdIns4P are defined and evidence that the majority of this lipid resides in the plasma membrane is presented, where it is metabolically distinct from the steady-state plasma membrane pool of PTDIns(4,5)P2. Expand
Direct Interaction of the Rab3 Effector RIM with Ca2+Channels, SNAP-25, and Synaptotagmin*
TLDR
It is proposed that the Rab3 effector RIM is a scaffold protein that participates through its multiple binding partners in the docking and fusion of secretory vesicles at the release sites. Expand
Activation of MDA5 Requires Higher-Order RNA Structures Generated during Virus Infection
TLDR
An antibody to dsRNA is used to show that the presence of immunoreactivity in virus-infected cells does indeed correlate with the ability of RNA extracted from these cells to activate MDA5, and suggests that Mda5 activation requires an RNA web rather than simply long molecules of ds RNA. Expand
Purification and Characterization of the Human Elongator Complex*
TLDR
Several human homologues of the yeast Elongator subunits were identified as subunits of the human Elongators, including StIP1 (STAT-interacting protein1) and IKAP (IKK complex-associatedprotein), raising the possibility that this disease might be due to compromised ElongATOR function and therefore could be a transcription disorder. Expand
A mutation in dynein rescues axonal transport defects and extends the life span of ALS mice
TLDR
It is proposed that impaired axonal transport is a prime cause of neuronal death in neurodegenerative disorders such as ALS and crossing S OD1G93A mice with Loa/+ mice delays disease progression and significantly increases life span in Loa/SOD1G 93A mice. Expand
Deficits in axonal transport precede ALS symptoms in vivo
TLDR
An in vivo assay that allows the characterization of axonal transport in single axons in the intact sciatic nerve is used and identifies clear axonal Transport deficits in presymptomatic mutant mice, representing one of the earliest axonal pathologies in SOD1G93A mice. Expand
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