LIS1, CLIP-170's Key to the Dynein/Dynactin Pathway [PDF]
Molecular and Cellular Biology, 2002 CLIP-170 is a plus-end tracking protein which may act as an anticatastrophe factor. It has been proposed to mediate the association of dynein/dynactin to microtubule (MT) plus ends, and it also binds to kinetochores in a dynein/dynactin-dependent fashion, both via its C-terminal domain. This domain contains two zinc finger motifs (proximal and distal),
Casper C Hoogenraad +2 more
exaly +7 more sources
Structural basis for cytoplasmic dynein-1 regulation by Lis1 [PDF]
eLife, 2022 The lissencephaly 1 gene, LIS1, is mutated in patients with the neurodevelopmental disease lissencephaly. The Lis1 protein is conserved from fungi to mammals and is a key regulator of cytoplasmic dynein-1, the major minus-end-directed microtubule motor ...
John P Gillies +6 more
doaj +4 more sources
NudEL targets dynein to microtubule ends through LIS1 [PDF]
Nature Cell Biology, 2005 Dynein is a minus-end-directed microtubule motor with critical roles in mitosis, membrane transport and intracellular transport. Several proteins regulate dynein activity, including dynactin, LIS1 (refs 2, 3) and NudEL (NudE-like). Here, we identify a NUDEL homologue in budding yeast and name it Ndl1. The ndl1delta null mutant shows decreased targeting
John A Cooper
exaly +6 more sources
Lis1 is an initiation factor for dynein-driven organelle transport [PDF]
Journal of Cell Biology, 2012 The molecular motor cytoplasmic dynein is responsible for most minus-end–directed, microtubule-based transport in eukaryotic cells. It is especially important in neurons, where defects in microtubule-based motility have been linked to neurological ...
Egan, Martin +2 more
core +6 more sources
Capturing disease severity in LIS1-lissencephaly reveals proteostasis dysregulation in patient-derived forebrain organoids [PDF]
Nature CommunicationsLIS1-lissencephaly is a neurodevelopmental disorder marked by reduced cortical folding and severe neurological impairment. Although all cases result from heterozygous mutations in the LIS1 gene, patients present a broad spectrum of severity. Here, we use
Lea Zillich +21 more
doaj +2 more sources
HIV-1 Tat interacts with LIS1 protein [PDF]
Retrovirology, 2005 Background HIV-1 Tat activates transcription of HIV-1 viral genes by inducing phosphorylation of the C-terminal domain (CTD) of RNA polymerase II (RNAPII).
Turner Willie +7 more
doaj +4 more sources
A selective LIS1 requirement for mitotic spindle assembly discriminates distinct T-cell division mechanisms within the T-cell lineage [PDF]
eLife, 2022 The ability to proliferate is a common feature of most T-cell populations. However, proliferation follows different cell-cycle dynamics and is coupled to different functional outcomes according to T-cell subsets.
Jérémy Argenty +7 more
doaj +2 more sources
Responsible Genes for Neuronal Migration in the Chromosome 17p13.3: Beyond Pafah1b1(Lis1), Crk and Ywhae(14-3-3ε) [PDF]
Brain Sciences, 2021 The 17p13.3 chromosome region is often deleted or duplicated in humans, resulting in severe neurodevelopmental disorders such as Miller–Dieker syndrome (MDS) and 17p13.3 duplication syndrome.
Xiaonan Liu +3 more
doaj +2 more sources
Altered extracellular matrix structure and elevated stiffness in a brain organoid model for disease [PDF]
Nature CommunicationsThe viscoelastic properties of tissues influence their morphology and cellular behavior, yet little is known about changes in these properties during brain malformations.
Maayan Karlinski Zur +14 more
doaj +2 more sources