Results 201 to 210 of about 49,031 (262)

Recombinant Monoclonal Antibodies for Detecting the Tubulin Post‐Translational Modifications Glutamylation and Lysine‐40 Acetylation

open access: yesCytoskeleton, EarlyView.
ABSTRACT Post‐translational modifications (PTMs) to tubulin subunits in microtubule filaments are thought to comprise a component of the tubulin code that specifies microtubule functions in cell physiology and animal development. Acetylation of Lysine‐40 (K40) on α‐tubulin (αTub‐K40ac) and glutamylation of both α‐ and β‐tubulin are two tubulin PTMs of ...
Lynne Blasius   +6 more
wiley   +1 more source

In Vivo Cytoskeletal AMPA Receptor Transport Imaging in C. elegans

open access: yesCytoskeleton, EarlyView.
ABSTRACT Long‐distance intracellular transport of ionotropic glutamate receptors (iGluRs) is essential for proper excitatory synaptic function underlying learning and memory. Many neuropsychiatric and neurodegenerative conditions have abnormal iGluR transport and trafficking, leading to an intense interest in the mechanisms and factors regulating these
Michaelis A. K., Hoerndli F. J.
wiley   +1 more source

Expression, Purification, and Microscopy‐Based Assays for Engineered Recombinant Tyrosinated, Detyrosinated, and Δ2 Human Tubulin

open access: yesCytoskeleton, EarlyView.
ABSTRACT Microtubules are noncovalent polymers assembled from α/β tubulin dimers. Their structure, dynamics and interaction with effectors are regulated through the expression of diverse tubulin isotypes and chemically diverse posttranslational modifications, also known as the “tubulin code.” Understanding the biophysical correlates between tubulin ...
Jiayi Chen   +2 more
wiley   +1 more source

Expression of mutant TIE2 p.L914F during mouse development causes embryonic lethality and defects in vascular remodeling

open access: yesDevelopmental Dynamics, EarlyView.
Abstract Background Sporadic venous malformation (VM) is associated with the hyperactivating p.L914F mutation in TIE2, a receptor tyrosine kinase essential for vascular development. This mutation is not found in hereditary VM, suggesting incompatibility with life when expressed during early vascular development.
Lindsay J. Bischoff   +6 more
wiley   +1 more source

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