scholarly journals Light-activated rhodopsin induces structural binding motif in G protein   subunit

1998 ◽  
Vol 95 (8) ◽  
pp. 4270-4275 ◽  
Author(s):  
O. G. Kisselev ◽  
J. Kao ◽  
J. W. Ponder ◽  
Y. C. Fann ◽  
N. Gautam ◽  
...  
Keyword(s):  
G Protein ◽  
Binding Motif ◽  
Protein Subunit

Mutations in G-protein subunit [alpha]q(GNAQ) are not a cause of familial hypocalciuric hypercalcaemia

2015 ◽  
Author(s):  
Manish Modi ◽  
Treena Cranston ◽  
Angela Rogers ◽  
Sarah Howles ◽  
Caroline Gorvin ◽  
...  
Keyword(s):  
G Protein ◽  
Protein Subunit

scholarly journals DAPLE and MPDZ bind to each other and cooperate to promote apical cell constriction

2019 ◽  
Vol 30 (16) ◽  
pp. 1900-1910 ◽  
Author(s):  
Arthur Marivin ◽  
Mikel Garcia-Marcos
Keyword(s):  
G Protein ◽  
Cultured Cells ◽  
Apical Cell ◽  
Cell Junctions ◽  
Binding Motif ◽  
Apical Constriction ◽  
Protein Activation ◽  
Neuroepithelial Cells ◽  
Two Factors ◽  
Apical Junctions

Dishevelled-Associating Protein with a high frequency of LEucines (DAPLE) belongs to a group of unconventional activators of heterotrimeric G-proteins that are cytoplasmic factors rather than membrane proteins of the G-protein–coupled receptor superfamily. During neurulation, DAPLE localizes to apical junctions of neuroepithelial cells and promotes apical cell constriction via G-protein activation. While junctional localization of DAPLE is necessary for this function, the factors it associates with at apical junctions or how they contribute to DAPLE-mediated apical constriction are unknown. MPDZ is a multi-PDZ (PSD95/DLG1/ZO-1) domain scaffold present at apical cell junctions whose mutation in humans is linked to nonsyndromic congenital hydrocephalus (NSCH). DAPLE contains a PDZ-binding motif (PBM) and is also mutated in human NSCH, so we investigated the functional relationship between both proteins. DAPLE colocalized with MPDZ at apical cell junctions and bound directly to the PDZ3 domain of MPDZ via its PBM. Much like DAPLE, MPDZ is induced during neurulation in Xenopus and is required for apical constriction of neuroepithelial cells and subsequent neural plate bending. MPDZ depletion also blunted DAPLE-­mediated apical constriction of cultured cells. These results show that DAPLE and MPDZ, two factors genetically linked to NSCH, function as cooperative partners at apical junctions and are required for proper tissue remodeling during early stages of neurodevelopment.

scholarly journals Central role of G protein Gαi2 and Gαi2+ vomeronasal neurons in balancing territorial and infant-directed aggression of male mice

2019 ◽  
Vol 116 (11) ◽  
pp. 5135-5143 ◽  
Author(s):  
Anne-Charlotte Trouillet ◽  
Matthieu Keller ◽  
Jan Weiss ◽  
Trese Leinders-Zufall ◽  
Lutz Birnbaumer ◽  
...  
Keyword(s):  
G Protein ◽  
Sensory Neurons ◽  
Neural Activity ◽  
Parental Behavior ◽  
Vomeronasal Organ ◽  
Male Infant ◽  
Lateral Septum ◽  
Male Mice ◽  
Protein Subunit ◽  
Α Subunit

Aggression is controlled by the olfactory system in many animal species. In male mice, territorial and infant-directed aggression are tightly regulated by the vomeronasal organ (VNO), but how diverse subsets of sensory neurons convey pheromonal information to limbic centers is not yet known. Here, we employ genetic strategies to show that mouse vomeronasal sensory neurons expressing the G protein subunit Gαi2 regulate male–male and infant-directed aggression through distinct circuit mechanisms. Conditional ablation of Gαi2 enhances male–male aggression and increases neural activity in the medial amygdala (MeA), bed nucleus of the stria terminalis, and lateral septum. By contrast, conditional Gαi2 ablation causes reduced infant-directed aggression and decreased activity in MeA neurons during male–infant interactions. Strikingly, these mice also display enhanced parental behavior and elevated neural activity in the medial preoptic area, whereas sexual behavior remains normal. These results identify Gαi2 as the primary G protein α-subunit mediating the detection of volatile chemosignals in the apical layer of the VNO, and they show that Gαi2+ VSNs and the brain circuits activated by these neurons play a central role in orchestrating and balancing territorial and infant-directed aggression of male mice through bidirectional activation and inhibition of different targets in the limbic system.

scholarly journals Proteomic Differences in the Hippocampus and Cortex of Epilepsy Brain Tissue

2020 ◽  
Author(s):  
Geoffrey Pires ◽  
Dominique Leitner ◽  
Eleanor Drummond ◽  
Evgeny Kanshin ◽  
Shruti Nayak ◽  
...  
Keyword(s):  
Dentate Gyrus ◽  
Frontal Cortex ◽  
G Protein ◽  
Molecular Mechanisms ◽  
High Rate ◽  
Label Free ◽  
Protein Subunit ◽  
Unexpected Death ◽  
Hippocampal Ca1 ◽  
And Control

AbstractEpilepsy is a common neurological disorder affecting over 70 million people worldwide, with a high rate of pharmaco-resistance, diverse comorbidities including progressive cognitive and behavioral disorders, and increased mortality from direct (e.g., Sudden Unexpected Death in Epilepsy [SUDEP], accidents, drowning) or indirect effects of seizures and therapies. Extensive research with animal models and human studies provides limited insights into the mechanisms underlying seizures and epileptogenesis, and these have not translated into significant reductions in pharmaco-resistance, morbidities or mortality. To help define changes in molecular signaling networks associated with epilepsy, we examined the proteome of brain samples from epilepsy and control cases. Label-free quantitative mass spectrometry (MS) was performed on the hippocampal CA1-3 region, frontal cortex, and dentate gyrus microdissected from epilepsy and control cases (n=14/group). Epilepsy cases had significant differences in the expression of 777 proteins in the hippocampal CA1-3 region, 296 proteins in the frontal cortex, and 49 proteins in the dentate gyrus in comparison to control cases. Network analysis showed that proteins involved in protein synthesis, mitochondrial function, G-protein signaling, and synaptic plasticity were particularly altered in epilepsy. While protein differences were most pronounced in the hippocampus, similar changes were observed in other brain regions indicating broad proteomic abnormalities in epilepsy. Among the most significantly altered proteins, G-protein Subunit Beta 1 (GNB1) was one of the most significantly decreased proteins in epilepsy in all regions studied, highlighting the importance of G-protein subunit signaling and G-protein–coupled receptors (GPCRs) in epilepsy. Our results provide insights into the molecular mechanisms underlying epilepsy, which may allow for novel targeted therapeutic strategies.

scholarly journals OR30-5 Germline Ablation of G-Protein Subunit Alpha-11 in Mice Causes Hypercalcemia That Is Rectified by Treatment with Cinacalcet

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Fadil Hannan ◽  
Mie Olesen ◽  
Tertius Hough ◽  
Michelle Stewart ◽  
Sara Wells ◽  
...  
Keyword(s):  
G Protein ◽  
Protein Subunit

scholarly journals Complexes of the G Protein Subunit Gβ5with the Regulators of G Protein Signaling RGS7 and RGS9

2000 ◽  
Vol 275 (32) ◽  
pp. 24872-24880 ◽  
Author(s):  
D. Scott Witherow ◽  
Qiang Wang ◽  
Konstatin Levay ◽  
Jorge L. Cabrera ◽  
Jeannie Chen ◽  
...  
Keyword(s):  
G Protein ◽  
G Protein Signaling ◽  
Protein Signaling ◽  
Protein Subunit
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