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we demonstrated that systemic administration of the small molecule CaMKK2 inhibitor, STO-609, to irradiated mice enhanced Hematopoietic stem and progenitor cells (HSPCs)recovery and improved survival. These findings identify CaMKK2 as an important regulator of HSPC regeneration and demonstrate CaMKK2 inhibition is a novel approach to promoting hematopoietic recovery after BM injury.
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loss of blood-brain barrier proteins, inactivation of survival gene expression such as B-cell lymphoma 2 (Bcl-2) and an increase in inflammatory cytokines in the serum were observed after stroke with CaMKK beta inhibition. We demonstrate that CaMKK beta is neuroprotective in stroke in aged mice
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CaMKK2 as a molecular rheostat for insulin action.
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CaMKK2 Inhibits C2C12 Myoblasts Proliferation and Differentiation through AMPK. Overexpression of CaMKK2 Inhibits Muscle Regeneration in Vivo.
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In summary, we demonstrate a new mechanism of calcium dependent antibacterial strategy in E. coli infected macrophages, which requires autophagy enhancement mediated by activation of CaMKKbeta, ERK, AMPK and FoxO1.
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CaMKKbeta exerts protective effects on cardiac adaptive energy pooling against pressure-overload possibly through phosphorylation of AMPK and by upregulation of PGC-1alpha.
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Results demonstrated that genetically inhibiting the CaMKK pathway via CaMKKbeta or CaMK IV is detrimental in the response of female mice to cerebral ischemia
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a novel function for CaMKK2 in bone remodeling and highlight the potential for its therapeutic inhibition as a valuable bone anabolic strategy that also inhibits OC differentiation in the treatment of osteoporosis.
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Flow-enhanced sirtuin (SIRT)1 stability is primarily mediated by CaMKKbeta phosphorylation of sirtuin SIRT1 at Ser-27 and Ser-47.
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amino acid starvation regulates autophagy in part through an increase in cellular Ca(2+) that activates a CaMKK-beta-AMPK pathway and inhibits mTORC1, which results in ULK1 stimulation
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Results suggest that in PCa progression, CaMKK2 and the AR are in a feedback loop in which CaMKK2 is induced by the AR to maintain AR activity, AR-dependent cell cycle control, and continued cell proliferation.
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an important function for CaMKK2 in mediating mechanisms that control the amplitude of macrophage inflammatory responses to excess nutrients or pathogen derivatives
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Suppressed catecholamine-induced induction of gluconeogenic gene expression in CaMKK2 knockout mice leads to improved whole-body glucose homeostasis despite the presence of increased hepatic fat content.
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a novel role for CaMKK2 as an inhibitor of granulocytic fate commitment and differentiation in early myeloid progenitors
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conclude that CaMKK2 and AMP-activated protein kinase function in a signaling pathway that participates in the regulation of adiposity
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findings suggest CaM kinase kinase beta isoforms are required for the formation of hippocampal long-term memory[LTM], but not needed for contextual, trace fear, and passive avoidance LTM
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Taken together, we conclude that CaMKKbeta has a male-specific function in hippocampal memory formation and we have identified male-restricted transcription occurring during hippocampal memory formation.
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contrasting phenotypes of the PSD-95 and Camkk2 mutant mice establish the prospect of an independent ,possibly, competing mechanism for the regulation of N-methyl-d-aspartate receptor dependent bidirectional synaptic plasticity
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CaMKK2/camkiv cascade involved in cerebellar granule cell development and show specifically that Ca(2+)-dependent regulation of BDNF through CaMKK2/CaMKIV is required for this process.
