scholarly journals Mutations in the β-Tubulin Gene TUBB5 Cause Microcephaly with Structural Brain Abnormalities

Cell Reports ◽  
2012 ◽  
Vol 2 (6) ◽  
pp. 1554-1562 ◽  
Author(s):  
Martin Breuss ◽  
Julian Ik-Tsen Heng ◽  
Karine Poirier ◽  
Guoling Tian ◽  
Xavier Hubert Jaglin ◽  
...  
Keyword(s):  
Brain Abnormalities ◽  
Tubulin Gene ◽  
Structural Brain ◽  
Β Tubulin

Structural brain abnormalities in the early phase of schizophrenia

2008 ◽  
Vol 23 ◽  
pp. S119-S120
Author(s):  
R. Herold ◽  
A. Feldmann ◽  
T. Tenyi ◽  
F. Kover ◽  
S. Fekete
Keyword(s):  
Early Phase ◽  
Brain Abnormalities ◽  
Structural Brain

scholarly journals Development and comparison of real-time and conventional PCR tools targeting β-tubulin gene for detection of Nosema infection in silkworms

2018 ◽  
Vol 43 (1) ◽  
pp. 31-38
Author(s):  
Vijaya Gowri Esvaran ◽  
Aarthi Mohanasundaram ◽  
Shruthi Mahadeva ◽  
Tania Gupta ◽  
Kangayam M. Ponnuvel
Keyword(s):  
Real Time ◽  
Conventional Pcr ◽  
Tubulin Gene ◽  
Nosema Infection ◽  
Β Tubulin

Neuroleptics in progressive structural brain abnormalities in psychiatric illness

The Lancet ◽  
1998 ◽  
Vol 352 (9130) ◽  
pp. 784-785 ◽  
Author(s):  
AL Madsen ◽  
N Keiding ◽  
A Karle ◽  
S Esbjerg ◽  
R Hemmingsen ◽  
...  
Keyword(s):  
Psychiatric Illness ◽  
Brain Abnormalities ◽  
Structural Brain

scholarly journals Structural brain abnormalities in epilepsy with myoclonic atonic seizures

2021 ◽  
pp. 106771
Author(s):  
Solange Denervaud ◽  
Christian Korff ◽  
Joël Fluss ◽  
Judith Kalser ◽  
Eliane Roulet-Perez ◽  
...  
Keyword(s):  
Brain Abnormalities ◽  
Atonic Seizures ◽  
Structural Brain

Functional analysis of the β 2 -tubulin gene of Fusarium graminearum and the β -tubulin gene of Botrytis cinerea by homologous replacement

2013 ◽  
Vol 69 (5) ◽  
pp. 582-588 ◽  
Author(s):  
ShengMing Liu ◽  
YaBing Duan ◽  
ChangYan Ge ◽  
ChangJun Chen ◽  
MingGuo Zhou
Keyword(s):  
Functional Analysis ◽  
Botrytis Cinerea ◽  
Fusarium Graminearum ◽  
Tubulin Gene ◽  
Β Tubulin

Structural brain abnormalities are related to retinal nerve fiber layer thinning and disease duration in neuromyelitis optica spectrum disorders

2014 ◽  
Vol 20 (9) ◽  
pp. 1189-1197 ◽  
Author(s):  
Felipe von Glehn ◽  
Sven Jarius ◽  
Rodrigo Pessoa Cavalcanti Lira ◽  
Maria Carolina Alves Ferreira ◽  
Fadua H Ribeiro von Glehn ◽  
...  
Keyword(s):  
Nerve Fiber ◽  
Neuromyelitis Optica ◽  
Retinal Nerve Fiber Layer ◽  
Disease Duration ◽  
Diffusion Tensor ◽  
Brain Abnormalities ◽  
Fiber Layer ◽  
Spectrum Disorders ◽  
And Diffusion ◽  
Structural Brain

Background: Although aquaporin-4 (AQP4) is widely expressed in the human brain cortex, lesions are rare in neuromyelitis optica (NMO) spectrum disorders (NMOSD). Recently, however, several studies have demonstrated occult structural brain atrophy in NMO. Objective: This study aims to investigate magnetic resonance imaging (MRI) patterns of gray matter (GM) and white matter (WM) abnormalities in patients with NMOSD and to assess the visual pathway integrity during disease duration correlation of the retinal nerve fiber layer (RNFL) and pericalcarine cortex thickness. Methods: Twenty-one patients with NMOSD and 34 matched healthy controls underwent both high-field MRI (3T) high-resolution T1-weighted and diffusion-tensor MRI. Voxel-based morphometry, cortical analyses (Freesurfer) and diffusion-tensor imaging (DTI) analyses (TBSS-FSL) were used to investigate brain abnormalities. In addition, RNFL measurement by optic-coherence tomography (OCT) was performed. Results: We demonstrate that NMOSD is associated with GM and WM atrophy, encompassing more frequently the motor, sensory and visual pathways, and that the extent of GM atrophy correlates with disease duration. Furthermore, we demonstrate for the first time a correlation between RNFL and pericalcarine cortical thickness, with cortical atrophy evolving over the course of disease. Conclusions: Our findings indicate a role for retrograde and anterograde neurodegeneration in GM atrophy in NMOSD. However, the presence atrophy encompassing almost all lobes suggests that additional pathomechanisms might also be involved.

P.0278 Structural brain abnormalities associated with cognitive impairments in bipolar disorder

2021 ◽  
Vol 53 ◽  
pp. S201
Author(s):  
J. Macoveanu ◽  
K.O. Freeman ◽  
H.L. Kjærstad ◽  
G.M. Knudsen ◽  
L.V. Kessing ◽  
...  
Keyword(s):  
Bipolar Disorder ◽  
Cognitive Impairments ◽  
Brain Abnormalities ◽  
Structural Brain

GENETICS OF THE TUBULIN GENE FAMILIES OF PHYSARUM

Genetics ◽  
1984 ◽  
Vol 108 (1) ◽  
pp. 143-164
Author(s):  
Tim Schedl ◽  
Judi Owens ◽  
William F Dove ◽  
Timothy G Burland
Keyword(s):  
Drug Resistance ◽  
Genetic Mapping ◽  
Gene Family ◽  
Gene Families ◽  
Resistance Locus ◽  
Tubulin Gene ◽  
Length Polymorphisms ◽  
Mapping Analysis ◽  
Mendelian Analysis ◽  
Β Tubulin

ABSTRACT The organization of the α- and β-tubulin gene families in Physarum was investigated by Mendelian analysis. Restriction endonuclease-generated DNA fragments homologous to α- and β-tubulin show length polymorphisms that can be used as markers for genetic mapping. Analysis of meiotic assortment among progeny of heterozygotes allowed α- and β-tubulin sequence loci to be defined. There are four unlinked α-tubulin sequence loci (altA, altB, altC and altD) and at least three unlinked β-tubulin sequence loci (betA, betB and betC). The α-tubulin loci are not linked to the β-tubulin loci. —Segregation of tubulin sequence loci with respect to ben mutations that confer resistance to antitubulin benzimidazole drugs was used to investigate whether any members of the α- or β-tubulin gene families are allelic to ben loci. The β-tubulin sequence locus betB is allelic to the resistance locus benD, the betA locus is probably allelic to benA and the α-tubulin sequence locus altC may be allelic to benC. The molecular implications of benzimidazole resistance phenotypes when only one of the expressed β-tubulin gene family members mutates to drug resistance are discussed in relation to tubulin function.

Sign in / Sign up

Export Citation Format

Share Document