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These results delineate a role for Galphai2 in early thymocyte development and for Galphai2/3 in multiple aspects of T cell biology.
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In conclusion, Galphai2 deficiency in erythrocytes confers partial protection against suicidal cell death.
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This study reveals how RGS proteins modulate Galphai2 signaling to facilitate thymocyte egress and T cell trafficking.
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this study shows that Galphai2 controls arrest in response to chemokine stimulation of neutrophils
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In Galphai2-knockdown mice, they showed defects in social interaction, novelty recognition and active avoidance learning.
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Data show that inhibitory (Galphai2) and stimulatory (GalphasL) G-protein subunits produced minor atrophic and hypertrophic changes in muscle mass, and Galphai2 over-expression prevented AAV:beta2-adrenoceptor (beta2-AR) mediated hypertrophy.
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RGS proteins and Galphai2 play a significant role in regulating states of wakefulness, NREM sleep, and REM sleep
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Kinocilium is essential for proper localization of Lgn, as well as Gai and aPKC, suggesting that cilium function plays a role in positioning of apical proteins critical for hearing.
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Galphai2 deficiency combined with cardiac beta1-adrenoceptor overexpression strongly impaired survival and cardiac function, leading to dilated cardiomyopathy.
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An essential role for Galpha(i2) in Smoothened-stimulated epithelial cell proliferation in the mammary gland.
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Platelet Galphai2 not only controls hemostatic and thrombotic responses but also is critical for the development of ischemia/reperfusion injury in vivo.
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Data show that disrupting resistance to inhibitors of cholinesterase 8A (Ric-8A) expression in hematopoietic cells results in a loss of GTP-binding protein alpha subunits Galphai2, Galphai3, and Galphaq.
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S1P sensitizes ICAPS through G-protein coupled S1P1 receptor activation of Galphai-PI3K-PKC-p38 signaling pathway in sensory neurons
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Myocardial ischemia promptly regulated cardiac mRNA and with a slight delay protein levels of both Galphai2 and Galphai3, indicating important roles for both Galphai isoforms.
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RGS protein/Galphai2 interactions have an essential role in B lymphocyte-directed cell migration and trafficking.
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Data (including data from knockout mice) suggest that Gnai2 in islet beta-cells is necessary for up-regulation of insulin secretion in response to high glucose in presence of L-arginine or L-ornithine.
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The absence of Galphai2 and Galphai3 in B cells profoundly disturbs the architecture of lymphoid organs with loss of B cell compartments in the spleen, thymus, lymph nodes, and gastrointestinal tract.
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Galphai2(Q205L) regulates satellite cell differentiation into myotubes in a protein kinase C - and histone deacetylase -dependent manner
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Galphas- and Galphai2-mediated signaling in the sinoatrial node is important in the reciprocal regulation of heart rate through the autonomic nervous system.
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Galphai2-deficient mice spontaneously develop colitis and colonic neoplasms the severity of which are determined by the interplay between Th1 and Th2 cell pathways.
