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Galpha11 is inhibitory to osteoanabolic actions of both parathyroid hormone and exercise
results suggest that alveolar Gq/11 signaling maintains alveolar homeostasis and likely independently increases TGFbeta activation in response to the mechanical stress of the epithelium and decreases epithelial IL-33 synthesis. Together, these findings suggest that disruption of Gq/11 signaling promotes inflammatory emphysema but protects against mechanically induced lung injury.
the results have identified 138 and 150 ovarian genes that are up-regulated or down-regulated, respectively, at the end of gestation in a Galphaq/11-dependent fashion.
In Galpha11-knock-out mice there is a decreased heart rate and increased ejection fraction.
claudin-3 and claudin-5 expression is increased by DHEAS and tight junction formation is stimulated via a Gnalpha11-coupled receptor in Sertoli cells
ZIP9/Gna11 interactions mediate the non-classical testosterone signaling cascade in spermatogenic GC-2 cells.
the conditional deletion of Galphaq/11 from granulosa/luteal cells prevents the progesterone withdrawal that occurs at the end of pregnancy and impairs parturition.
Loss of gq/11 genes does not abolish melanopsin phototransduction.
Mediated by lysophosphatidylinositol, Galpha(q/11) is activated in sensory neurons.
Dehydroepiandrosterone sulfate (DHEAS)-induced signaling is mediated through interaction with a membrane-bound G-protein-coupled receptor, since silencing of Gnalpha11 leads to the abolition of the DHEAS-induced stimulation of Erk1/2, ATF-1, and CREB.
Pasteurella multocida toxin prevents osteoblast differentiation by transactivation of the MAP-kinase cascade via the Galpha(q/11)--p63RhoGEF--RhoA axis.
Myocytes from the Galpha(q) and/or Galpha(11) KO mice displayed genuine alterations in the action potentials, membrane capacitance, membrane currents, and Ca(2+) handling
Report differential expression of protein kinase C isoforms in coronary arteries of diabetic mice lacking Gna11.
GPR54 regulates ERK1/2 activity and hypothalamic gene expression in a Galpha(q/11) and beta-arrestin-dependent manner.
a signaling pathway via the G(q)-proteins, G(alpha)(11) and G(alpha)(q), that could link increased neurohumoral stimulation in diabetes with defective RyR2 channel function by regulating protein expression of FKBP12.6, annexin A7, and sorcin.
Galpha(q) and Galpha(11) proteins serve as the intracellular mediators of endothelin-1 signaling in the pharyngeal arch mesenchyme
Our findings suggest an expression level-dependent action of Galpha(q) and Galpha11 for Purkinje cell signaling and assign specific roles of these two G(q) isoforms for motor coordination
G(q/11) signaling is indispensable to the neuronal circuit that connects the perception of pup-related stimuli to the initiation of maternal behavior
G(q)/G(11)- but not G(12)/G(13)-mediated signaling processes mediate ET-1/ET(A)-dependent development of the cephalic neural crest.
both Gq and G11 have critical roles in mediating inhibition of PTH secretion by extracellular Ca2+
Results show that postzygotic mosaicism for GNA11 mutations causes an overlapping phenotypic spectrum of vascular and melanocytic birthmarks.
GNAQ/GNA11Q209 mutations characterized a distinct, albeit uncommon subtype of non-uveal melanoma (0.5-1%). These mutations were essentially melanoma-specific, occurred in all subtypes of this disease (including cutaneous, mucosal, uveal, and unknown primary), and were mutually exclusive with other common melanoma mutations.
GNA11 mutations are associated with extremity capillary malformations causing overgrowth.
There were no significant differences in the prevalence of GNAQ and GNA11 mutations between patients with or without metastatic disease
a novel germline gain-of-function Galpha11 mutation, Val340Met, causing Autosomal Dominant Hypocalcemia Type 2 demonstrates the importance of the Galpha11 C-terminal region for G-protein function and CaSR signal transduction.
studies have identified a third Galpha11 mutation (Thr54Met) causing Familial Hypocalciuric Hypercalcemia Type 2 and reveal a critical role for the Galpha11 interdomain interface in CaSR signaling and Ca(2+) o homeostasis.
Adenocarcinomas or adenomas derived from pigmented ciliary epithelium is distinguished from uveal melanoma by the absence of SOX10 expression and presence of the BRAF V600E mutation.
Mutations in GNAQ and GNA11 genes in Greek uveal melanoma population present frequencies that qualify them as potential targets for customized therapy.
Sporadic melanotic schwannoma with overlapping features of melanocytoma bearing a GNA11 mutation in an adolescent girl.
we find iris melanomas to be related genetically to choroidal and ciliary body melanomas, frequently harboring GNAQ, GNA11, and EIF1AX mutations.
GNAQ and GNA11 mutations occur frequently in mucosal melanoma and may be a prognostic factor for MM. Our data implicate that GNAQ/11 may be potential targets for targeted therapy of mucosal melanoma.
CGRP family of receptors displays both ligand- and RAMP-dependent signaling bias among the Galphas, Galphai, and Galphaq/11 pathways.
The identified GNA11 mutation results in biochemical abnormalities typical for autosomal dominant hypocalcemia. Additional features, including short stature and early intracranial calcifications, cosegregated with the mutation.
In 33 CASR-negative patients with suspected FHH, Data found two (~6%) with a mutation in AP2S1 (p.Arg15Leu and p.Arg15His). Family screening confirmed the genotype-phenotype correlations. Data did not identify any pathogenic mutations in GNA11.
Driver mutations are rare in mutational hotspots of BRAF, NRAS, KIT, and GNAQ/GNA11 in oral mucosal melanoma.
These findings demonstrate that CaSR-targeted compounds can rectify signaling disturbances caused by germline and somatic Galpha11 mutations, which respectively lead to calcium disorders and tumorigenesis; and that ADH2-causing Galpha11 mutations induce non-constitutive alterations in MAPK signaling.
Mutations in GNA11 gene is associated with malignant uveal melanoma.
extensive dermal melanocytosis and phakomatosis pigmentovascularis are associated with activating mutations in GNA11 and GNAQ, genes that encode Galpha subunits of heterotrimeric G proteins
Melanomas associated with blue nevi or mimicking cellular blue nevi commonly have GNA11 mutations.
Distribution of GNAQ and GNA11 Mutation Signatures in Uveal Melanoma Points to a Light Dependent Mutation Mechanism.
The phylogenetic trees reveal that porcine Gna11, is evolutionarily close to the human homolog.
G protein-coupled receptor Kinase 2 reacts with this protein's signaling homology domain for binding G protein subunits
Melanopsin photostimulation triggers the phosphoinositide pathway through activation of a G-Protein, G11.
may be involved in mediating second messenger signals from the endothelin receptor in adipocytes
G-protein subunit alpha-11
, g alpha-11
, guanine nucleotide-binding protein subunit alpha-11
, guanine nucleotide regulatory protein G alpha 11
, guanine nucleotide-binding protein alpha 11 subunit
, guanine nucleotide-binding protein G(y) subunit alpha
, guanine nucleotide-binding protein, Gq class, GNA11
, G alpha-11
, Guanine nucleotide-binding protein alpha-11 subunit
, guanine nucleotide binding protein alpha 11
, G-protein subunit GL2 alpha
, phospholipase C-activating G-protein
, Galpha 11b
, guanine nucleotide binding protein (G protein), alpha 11 (Gq class)
, guanine nucleotide binding protein (G protein), alpha 11a (Gq class)
, guanine nucleotide binding protein (G protein), alpha 11 (Gq class) S homeolog
, guanine nucleotide binding protein, alpha 11
, Galpha 11a