The differential distribution of beta tubulin mRNAs in individual mammalian brain cells

1985 ◽  
Vol 27 (3) ◽  
pp. 205-214 ◽  
Author(s):  
W. Sue T. Griffin ◽  
Michael A. Alejos ◽  
Erica J. Cox ◽  
Marcelle R. Morrison
Marine Drugs ◽  
2015 ◽  
Vol 13 (2) ◽  
pp. 920-935 ◽  
Author(s):  
Thorsten Mordhorst ◽  
Sushil Awal ◽  
Sebastian Jordan ◽  
Charlotte Petters ◽  
Linda Sartoris ◽  
...  

2018 ◽  
Vol 29 (5) ◽  
pp. 575-586 ◽  
Author(s):  
Julbert Caneus ◽  
Antoneta Granic ◽  
Rosa Rademakers ◽  
Dennis W. Dickson ◽  
Christina M. Coughlan ◽  
...  

Mutant Tau (MAPT) can lead to frontotemporal lobar degeneration (FTLD). Previous studies associated MAPT mutations and altered function with aneuploidy and chromosome instability in human lymphocytes and in Drosophila development. Here we examine whether FTLD-causing mutations in human MAPT induce aneuploidy and apoptosis in the mammalian brain. First, aneuploidy was found in brain cells from MAPT mutant transgenic mice expressing FTLD mutant human MAPT. Then brain neurons from mice homozygous or heterozygous for the Tau (Mapt) null allele were found to exhibit increasing levels of aneuploidy with decreasing Tau gene dosage. To determine whether aneuploidy leads to neurodegeneration in FTLD, we measured aneuploidy and apoptosis in brain cells from patients with MAPT mutations and identified both increased aneuploidy and apoptosis in the same brain neurons and glia. To determine whether there is a direct relationship between MAPT-induced aneuploidy and apoptosis, we expressed FTLD-causing mutant forms of MAPT in karyotypically normal human cells and found that they cause aneuploidy and mitotic spindle defects that then result in apoptosis. Collectively, our findings reveal a neurodegenerative pathway in FTLD-MAPT in which neurons and glia exhibit mitotic spindle abnormalities, chromosome mis-segregation, and aneuploidy, which then lead to apoptosis.


2010 ◽  
Vol 1 (1) ◽  
pp. 3-15 ◽  
Author(s):  
Javier Márquez ◽  
Mercedes Martín-Rufián ◽  
Juan A. Segura ◽  
José M. Matés ◽  
José A. Campos-Sandoval ◽  
...  

AbstractGlutaminase is considered as the main glutamate producer enzyme in brain. Consequently, the enzyme is essential for both glutamatergic and gabaergic transmissions. Glutamine-derived glutamate and ammonia, the products of glutaminase reaction, fulfill crucial roles in energy metabolism and in the biosynthesis of basic metabolites, such as GABA, proteins and glutathione. However, glutamate and ammonia are also hazardous compounds and danger lurks in their generation beyond normal physiological thresholds; hence, glutaminase activity must be carefully regulated in the mammalian brain. The differential distribution and regulation of glutaminase are key factors to modulate the metabolism of glutamate and glutamine in brain. The discovery of novel isoenzymes, protein interacting partners and subcellular localizations indicate new functions for brain glutaminase. In this short review, we summarize recent findings that point consistently towards glutaminase as a multifaceted protein able to perform different tasks. Finally, we will highlight the involvement of glutaminase in pathological states and its consideration as a potential therapeutic target.


1988 ◽  
Vol 7 (8) ◽  
pp. 2311-2319 ◽  
Author(s):  
R. D. Burgoyne ◽  
M. A. Cambray-Deakin ◽  
S. A. Lewis ◽  
S. Sarkar ◽  
N. J. Cowan

2019 ◽  
Vol 29 (4) ◽  
pp. 51-56
Author(s):  
A. S. Yakimov ◽  
◽  
E. D. Osipova ◽  
A. V. Morgun ◽  
E. B. Boytsova ◽  
...  

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