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AKT activates cell differentiation. 826 / 841
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"Despite genes in module 1 were shared by both SPC and EC-2 populations, a large number of genes associated with PI3K/AKT/mTOR pathway were significantly increased during c-Kit SPC differentiation process, which indicates the activation state of this pathway.To further confirm the activation state and essential role of AKT/mTOR pathway in this process, we next investigated whether AKT/mTOR pathway may modulate cellular metabolism as well as vascular c-Kit SPC differentiation in vitro, using isolated vascular c-Kit SPCs described above."
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"The functions of Akt in embryonic stem cells (ESCs) XREF_BIBR, adult stem cells XREF_BIBR and cancer stem cells (CSCs) XREF_BIBR have been investigated, but its precise role in the maintenance of stem cell homeostasis and the mechanism by which Akt modulates differentiation are yet to be clarified."
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"A significant decrease in the p-Akt and Akt ratio was observed in syringin treated cells compared to that of the control (XREF_FIG C); it has been reported that inhibition of Akt phosphorylation and activation blocks adipocyte differentiation of 3T3-L1 cells, and suggests syringin 's ability to inhibit the Akt activation [XREF_BIBR, XREF_BIBR]."
| PMC
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"Icariside II treatment increases the phosphorylation level of Akt and S6K1 in BM-MSCs and promotes the osteogenic differentiation of MSC through PI3K/Akt/mTOR/S6K1 signaling pathway.152 Risedronate can inhibit the phosphorylation of downstream effectors of mTOR and impair the adipogenic differentiation of MSCs.106 Under hypoxic preconditioning, HIF-1α-mediated 78 kDa glucose regulatory protein (GRP78) regulates the activation of Akt, mTOR, and p70S6k, and the expression of cell cycle–related proteins increases through the GRP78–Akt axis."
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"In various cell types activation of Ras leads to activation of the mitogen activated protein kinases (MAPKs), extracellular signal regulated kinase 1/2 (ERK1/2), and protein kinase B (PKB)/Akt, which exert opposing effects on adipogenesis, with ERK1/2 inhibiting and PKB and Akt promoting terminal differentiation."
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"In various cell types activation of Ras leads to activation of the mitogen activated protein kinases (MAPKs), extracellular signal regulated kinase 1/2 (ERK1/2), and protein kinase B (PKB)/Akt, which exert opposing effects on adipogenesis, with ERK1/2 inhibiting and PKB and Akt promoting terminal differentiation."
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"M-CSF receptor is expressed at low levels on HSCs and at higher levels on monocytes and tissue Mϕs. Its ligation activates PI3K/AKT, Src, PLC-γ, and ERK kinases and SHP-1 phosphatase, promoting cell survival, proliferation, and differentiation (Sherr, 1990; Jack et al., 2009; Stanley and Chitu, 2014) ."
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"Notably, in a randomized controlled study, Xuezhikang combined with anti-hypertensive treatment could result in benefits independent of blood pressure-lowering effects in patients with essential hypertension controlled by anti-hypertensive medications by increasing the number of CEPCs and improving CEPCs mobilization and differentiation from bone marrow, promoting their migration and differentiation by phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt) signal conduction pathway, preventing CEPCs senescence by modulating cellular cycling related proteins, and up-regulating the expression of the integrin in CEPCs to enhance their adherent and migratory capacities70.5.6
Protection against liver disorders."
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"The first cocktail contains compounds that activate Wnt, AMPK and PKB and AKT signaling to stimulate proliferation, survival and the insulin response, while the second cocktail includes small molecules that prevent apoptosis and promote hematopoietic differentiation (i.e. DITPA or VEGF inducer)."
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"1 The activated HER2 protein recruits and regulates various intracellular signaling proteins PI3K/Akt, JAK2, STAT3 and STAT5 to induce cancer cell proliferation, differentiation, and survival in HER2 BC.54–56 Trastuzumab treatment has been shown to block HER2-mediated PI3K/Akt signaling activation in HER2 BC cells."
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"Targets in downstream or resistant pathways of particular interest in HER2-positive breast cancer include mTOR, PI3K, IGF-1R, Akt, HSP90, and VEGF that allow cell development, survival, and differentiation (Agus et al., 2005; Arteaga et al., 2012; Franklin et al., 2004; Nahta et al., 2006)."
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"VEGF2 treated EPCs have enhanced AKT activation, and infarcted hearts receiving these VEGF-2 treated EPCs exhibit improved angiogenesis and cardiac function compared with control treated hearts, while inhibition of AKT by Ox-LDL impairs endothelial differentiation in bone marrow stem cells."
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"During keratinocyte differentiation, the activation of PI3K pathway, which depends on the activity of EGFR, Fyn/Src kinases, and E-cadherin-mediated adhesion, actually initiates AKT activation, which in turn, promotes the growth arrest and differentiation of keratinocytes, as evidenced by increased expression of filaggrin, loricrin, keratin 1, and keratin 5."
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"Bone destruction in RA is mainly mediated by osteoclasts, and persistent joint inflammation enhances the differentiation and activity of osteoclasts and impairs the differentiation and function of osteoblasts, leading to imbalance of bone homeostasis and bone destruction.74 Within osteoclasts, RANKL interacts with cytokines to phosphorylate downstream PKB/AKT in the cytoplasm and promotes the formation of osteoclasts."
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"To unveil the molecular mechanisms through which KYMASIN UP exerted its effects on OBs and OCs, we investigated several intracellular signaling pathways, i.e., Src (non-receptor tyrosine kinase), p38 MAPK (mitogen-activated protein kinase), ERK1/2 (extracellular signal-regulated kinases), and AKT (protein kinase B), which have been involved in RANKL-dependent osteoclastogenesis and BMP2-induced OB differentiation [41,42]."
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"Akt signals downstream of PI3 kinase, and direct inhibition of either of these proteins causes differentiation of hESCs [XREF_BIBR, XREF_BIBR], as does inhibition of FKBP12-rapamycin-associated protein and mechanistic target of rapamycin (kinase), which signals downstream of Akt [XREF_BIBR]."
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"As reported, zinc could optimize anti-tumour effects by inhibiting LPS-, ROS- or other immune factor induced oncogenic signalling pathways, such as NF-kappaB, activator protein-1, Janus tyrosine kinase and signal transducer and activator of transcription (JAK and STAT), and PI3K and Akt; decrease oxidative stress and inflammatory responses induced by chemo- and radiotherapy; promote the development and differentiation of T and B lymphocytes; and improve the tumour microenvironment to reduce the risk of prostate, oesophageal, lung, and oral cancers [XREF_BIBR - XREF_BIBR]."
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"Under the action of a catalytic subunit, the downstream effector molecule Akt gets activated, followed by the activation of the downstream target gene to promote the differentiation and proliferation of spermatogonial stem cells and the occurrence of sperms (He et al., 2009) (Supplementary Figure S1)."
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"As Activin/Smad2/3 signaling is required for expression of the pluripotency gene Nanog, these results suggest that robust PI3K and Akt activity collaborates with Activin and Smad signaling to maintain hESC self-renewal, while weak PI3K and Akt activity switches the function of Activin and Smad to promote differentiation."
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"92 Additionally, Vu et al. found that m A mediated by METTL3 promoted the translation of c‐MYC, BCL2 and PTEN mRNAs, and the PTEN transcript may encode a negative regulator of p‐AKT which was considered to promote differentiation and inhibit self‐renewal.93
Although METTL3 was previously thought to be down‐regulated in GSCs, the concept has become controversial."
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"In addition, Studies have shown that PI3K-Akt signaling positively regulates Th17 differentiation via multiple mechanisms including the regulation of hypoxia inducible factor 1alpha (HIF-1 alpha) expression, Signal transducer and activator of transcription 3 (STAT3) phosphorylation, Gfi1 downregulation, and the nuclear translocation of RORgammat [XREF_BIBR - XREF_BIBR]."
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"Whereas AKTi treated CD34 + cells showed enhanced B-lineage reconstitution compared with the control group, inhibition of AKT activity decreased T-cell and myeloid differentiation of CD34 + cells (XREF_FIG), which is consistent with the in vitro liquid culture experiment shown in XREF_FIG."
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"Contrary to P-ERK effect, some reports said that the activated PI3K/AKT signal channel could promote differentiation of Schwann cells and also believed that the significantly activated ERK and the activity-enhanced AKT joint played important roles in inducing activation and proliferation process of Schwann cells at the early state of nerve injury (Ogata et al., 2004)."
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"These results suggest that the PI3K and Akt signaling pathway can promote proliferation and adipogenic differentiation of adipose stem cells, and that activation of this pathway by FGF2 may explain why hbASCs show greater proliferation and adipogenic differentiation than haASCs and htASCs."
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"It has already been demonstrated that the PI3K/Akt and MAPK (ERK1/2) pathways promote glucose transport, cell proliferation, and cell differentiation; follicular apoptosis interacts with gonadotropins to modulate ovarian hormone secretion [55,56,57], in addition to being related to mitochondrial function in the ovary [58]."
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"Terminal adipocyte differentiation is promoted by the activity of several kinases, particularly kinases of the PI3K and AKT pathway and those activating p38 mitogen activated protein kinases, and results in the synthesis of adipocyte secreted products, including adiponectin (the most abundant transcript in human adipose tissue) and leptin."
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"Notably, the PI3K/AKT signaling pathway is one of the most common pathways downstream of the receptor tyrosine kinases and is involved in the regulation of numerous cellular activities, including cell growth, migration, differentiation, apoptosis, and energy metabolism AKT is activated by the PI3K/AKT pathway and regulates tumor progression."
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"Of note, Akt kinases, also known as protein kinase B, are signaling molecules of cell growth and differentiation and serve as a well-characterized effector of phosphoinositide 3-kinase (PI3K), involved in diverse cellular processes, especially for inflammation.141,153,154 As indicated by Xia et al69 and Wang et al,89 given that Neat1 can modify miRNA/PI3K/AKT axis in cell and animal models exposed to inflammation, it exhibited great potential in inflammatory conditions treatment."
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"To confirm whether the CTGF treatment induced hESC differentiation into MSCs and can modulate the Wnt–β-catenin signaling, cell survival/apoptosis-related signaling molecules, and growth factors related with CTGF during differentiation, we performed immunoblotting analysis for TGF-β, β-catenin, JNK/p38, and AKT during the CTGF-induced differentiation of the hESCs."
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"There are similar intracellular segments in different receptor families, which regulate similar signaling pathways and exhibit similar functions, including activation of the PI3/Akt and Erk1/2 signaling pathways to promote cell proliferation, differentiation, migration, and cell cycle progression (16)."
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"Finally, by means of its insulin-mimetic property, MYO should be able to stimulate the expression of cell surface receptors for TGFbeta, which are necessary for TGFbeta/Akt-mediated endothelial migration and differentiation during revascularization (Hata and Chen, 2016; Budi et al., 2019)."
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"For example, microspheres of hydroxyapatite-modified hydrogels facilitated force transmission by mimicking the high mechanical strength of bone regeneration ECM and further activated signalling pathways such as Wnt/β-catenin and PI3K/Akt promoting the proliferation of BMSCs and differentiation into bone."
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"Because increased levels of PI3K, Akt, mTOR, and metabolic activities support Th17 cell differentiation and inhibit Treg differentiation XREF_BIBR, XREF_BIBR, XREF_BIBR, we examined the possibility that increased expression or activity of RARalpha favors the differentiation of Th17 over that of Treg cells."
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"Using CD8 + T cells from pdk1 K465E and K465E knockin mice, we found that decreased Akt activity inhibited the survival of T cells during the effector-to-memory cell transition and abolished their differentiation into C-X-C chemokine receptor 3 (CXCR3) lo CD43 lo effector like memory cells."
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"Overall, activating mutations of PI3K and AKT genes appear to cause profound disturbances of cellular proliferation, differentiation, and growth, reflecting the central role of these enzymes in development, and the widespread expression of the cognate genes in progenitors, neurons, and glia."
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"For example, Wnt and beta-catenin and Akt signaling are inhibited by miRNAs to attenuate osteogenic differentiation of MSCs, Notch and NF-kappaB signaling are hindered to suppress the chondrogenic differentiation of MSCs, and the cell cycle is blocked by miRNA via targeting CDK6 to promote adipogenic differentiation of MSCs."
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"Mechanistically, Pi retention is mediated by soluble carrier family 20 member 1 (SLC20A1) and sensed by diphosphoinositol pentakisphosphate kinase 2 (PPIP5K2) to enhance Akt activation, which then upregulates SLC20A1 to aggravate Pi retention and augments GATA2 activity to drive the expansion and megakaryocyte/myeloid-biased differentiation of HSCs."
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"The PI3K and Akt cell signaling cascade is commonly activated in many types of cancers, regulating cell survival, differentiation, proliferation, and apoptosis, and the inhibition of Akt phosphorylation has been deemed as a feasible strategy for the therapeutic treatment against human cancers."
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"Its down-regulation is directly linked to the reduced phosphorylation of AKT and PKC, which leads to an impaired differentiation of Th2 cells, producing IL-4, IL-5, IL-10, and IL-13, responsible for strong antibody production, eosinophil activation, and inhibition of several macrophage functions, providing phagocyte independent protective responses [XREF_BIBR]."
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"Like NGF, MT2 increased phosphorylation of extracellular signal regulated kinase1/2 and Akt proteins and production of MKP-1 phosphatase (dual specificity phosphatase 1), modulated p38 mitogen activated protein kinase activation, sustained survival of serum starved PC12 or RDG cells, and promoted their differentiation."
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"Given the key role of AKT activation in the transformation of hNSCs and endothelial lineage differentiation of GSC, coupling with the association of high-AKT activation with poor prognosis, we identified a list of genes associated with high AKT activation from our oncogene induced hNSC system (XREF_SUPPLEMENTARY)."
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"Our findings suggest that in young and adult mice TRAF3 forms a complex with PI3K to prevent AKT phosphorylation and degradation of β-catenin to enhance OB differentiation and maintain bone mass (Fig. 3), which is supported by our finding that TRAF3 over-expression increased OB differentiation [120]."
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"A series of studies demonstrated that constitutive Akt hyperactivity driven by the proteolipid protein (Plp) promoter enhances CNS myelination without affecting OPC proliferation, survival, and differentiation (Flores et al., 2008) and the myelination-promoting effect appears to act through mTOR signalling, one of the downstream substrates of Akt (Narayanan et al., 2009; Wahl et al., 2014), specifically through Raptor-containing mTOR complex 1 (mTORC1) (Bercury et al., 2014)."
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"The PI3K-AKT pathway plays a crucial role in adipogenesis, as pharmacological inhibition of the pathway blocks adipocyte differentiation
(Tomiyama et al., 1995; Xia & Serrero, 1999; Xu & Liao, 2004; Yu et al., 2008; Kim et al., 2009; Jacobsen et al., 2016)
and the expression of constitutively active AKT was shown to cause spontaneous differentiation into adipocytes
(Kohn et al., 1996; Magun et al., 1996)
."
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"These data demonstrate that PI3K and AKT inactivation stimulated melanoma GFP high cell differentiation, suggesting that TNF suppresses their commitment to the differentiation fate by activating AKT, consequently preventing asymmetric self-renewal and promoting symmetric self-renewal of GFP high melanoma SCs."
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"XREF_BIBR It has been established that Akt activation regulates the differentiation of CD8 + T cells into effector and memory T cells, where sustained Akt activation leads to terminal differentiation of effector CD8 + T cells, whereas inhibition of Akt in vivo increases the number of memory CD8 + T cells."
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"Interestingly, it has been shown that the PI3K and Akt signaling pathway plays a crucial role in many intracellular cascade events including tumor angiogenesis and tumor growth, and in particular, the PI3K and Akt pathway has been reported to drive the shear induced stem cell differentiation into ECs."
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"Combined with the results that Tfh cells had reduced Akt and mTOR signaling compared with Th1 cells in vivo and that overexpression of constitutively active Akt promoted Th1 cell differentiation, that study suggests that in addition to the IL-2/STAT5/Blimp1 axis, the IL-2/Akt/mTOR axis also favors Th1 cell development at the expense of Tfh cells 132."
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"To demonstrate whether Akt signalling mediates EPC differentiation, bone marrow derived cells from PPARalpha WT mice were incubated in the absence or presence of either MPs PPARalpha +/+ or MPs PPARalpha-/-, and Akt phosphorylation on Ser 473 indicative for Akt activity was detected by Western blot analysis."
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"XREF_BIBR Sustained Akt activation leads to terminal differentiation of effector CD8 + T cells, whereas inhibition of Akt in vivo increases the number of memory CD8 + T cells, XREF_BIBR and the downstream inhibition of mTOR augments the functional quality of cytotoxic CD8 + T-cell responses by prompting a CD8 memory phenotype."
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"In conclusion, we determined that transient TNF suppresses the PI3K and AKT mediated melanoma SC differentiation and enlarges a GFP high melanosphere initiating CSC subpopulation that preserves the TNF instigated changes, reinforcing their post-TNF capacity to form tumor like melanospheres."
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"The major findings of our study are that MPs PPARalpha +/+ : (i) increase EPC differentiation and EC marker expression, but not those of macrophage differentiation; (ii) enhances EPC differentiation that is mediated, at least in part, by PPARalpha-NF-kappaB and Akt pathways; (iii) modulate in vitro angiogenic related properties of ECs; and (iv) stimulate in vivo bone marrow derived cell associated neovascularization."
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"Furthermore, PKB phosphorylation promotes venous differentiation at the expense of arteriogenesis.Hereditary hemorrhagic telangiectasia (HHT; or Osler–Weber–Rendu syndrome) and cerebral cavernous malformation (CCM) result from lowered and elevated signaling from the TGFβ/ BMP receptor complexes and sensitivity to messengers, respectively [210]."
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"Akt is phosphorylated and activated via PI3K in response to signals originated by the erythropoietin (EPO) receptor; in particular, Akt is able to support erythroid differentiation in JAK2 deficient fetal liver progenitor cells through a mechanism downstream of EpoR XREF_BIBR and at least in part related to GATA-1 phosphorylation XREF_BIBR."
eidos
"6 In summary , OT and AVP activate a complex array of signaling pathways to regulate skeletal muscle homeostasis ( modulating different kinases , modifying the calcium level , through the CaMK / Calcineurin signaling to activate the myogenic regulatory factors expressions , and by stimulating the Akt / mTOR or the MAPK pathway to induce muscle cell proliferation , differentiation , contraction , and regeneration ."
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"Taken together with findings that constitutively active Akt is sufficient to induce adipocyte differentiation in vitro in the absence of hormones and Akt null mice display severe defects in adipocyte development, an Akt/FOXO1/PPARgamma driven lipogenesis mechanism has solid experimental support [XREF_BIBR, XREF_BIBR]."
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"XREF_BIBR and other studies have found that inhibition of AKT can limit in vitro MDSC differentiation, and XREF_BIBR discovered Treg is more susceptible to be inhibited after using AkT inhibitors, thus increasing CD8 + T cell number in tumor tissue to improve the control of tumor focus."
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"PIP3 thus functions as a second messenger initiating multiple signaling cascades, most notably facilitating the phosphorylation of AKT by PDK1 which subsequently leads to downstream survival and differentiation signals secondary to activation of the mechanistic target of rapamycin 1 (mTORC1) (40, 41) (Figure 1)."
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"In order to determine the purity of the primary astrocyte cultures and to investigate whether the expression of c-Myc and/or Akt induced the expression of neural differentiation markers we performed RPA with a probe set containing neuronal (GAP43, NF68, synaptophysin, calbindin), astrocytic (GFAP) and oligodendroglial (PLP, MBP) genes."
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"Because its Akt-activated overexpression induces neuronal differentiation and cell survival [88], p62 may be involved in various regulatory mechanisms and attenuate the onset of apoptosis, suggesting that alternative pathways may exist.The ATG family of proteins is involved in the formation and maturation of autophagosomes during autophagy [35], and disruption of its expression in neurons causes neuronal degeneration [89]."
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"Additional pathways induced by CCR5, include the PI-3 ' K pathway and thereby PDK1 and the serine/threonine kinase protein kinase B (AKT), which in turn induces cell survival, glycolysis, cell proliferation, growth and proliferation of progenitor and stem cells, immune cell differentiation and the release of eIF4E to promote cap dependent translation (XREF_FIG)."
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"33 Since it is well known that hypoxia and starvation associate with progression and drug resistance by inducing biological changes in tumor cells, one of them being increased glycolysis.35 Moreover, the C-terminal peptide of NSE, which is not related to glycolytic pathway, was demonstrated to promote survival, differentiation and regeneration of neuroblastoma cells by activation of the phosphatidylinositol-3-kinase/protein kinase B (AKT) and mitogen-activated protein kinase/ERK signal pathways."
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"Moreover, it was found that the activation of FPRs increased the generation of reactive oxygen species (ROS) and phosphorylation of AKT in the NSCs, while N-acetylcysteine and LY294002 inhibited the FPRs stimulated increase in ROS generation and AKT phosphorylation, and blocked the FPRs stimulated neural differentiation into neurons."
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"Akt is primarily responsible for the ability of insulin and IGFs to stimulate cell growth, survival, differentiation, and metabolic responses.Among downstream kinases in insulin/IGF signaling, the Ser/Thr kinase mechanistic target of rapamycin (mTOR) regulates many activities of insulin/IGF."
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"In addition, H. pylori activates multiple intracellular pathways in epithelial cells, such as the NF-κB, β-catenin pathway and PI3K/AKT pathway, which induces increased inflammatory cytokine production, altered apoptosis rate, and deregulated epithelial cell proliferation and differentiation, finally leading to the oncogenic transformation of early human gastric cancer (78, 82–88)."
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"Akt is a key component of insulin signaling and is required for PPARg expression.75,95 Over-expression of constitutively active Akt induces spontaneous differentiation of 3T3-L1 preadipocytes,96 and mice null for Akt1 and Akt2 have impaired adipogenesis.95 Akt is responsible for phosphorylation and nuclear exclusion of anti-adipogenic factors such as the forkhead proteins FOXO-197 and FOXO-2,98 and the transcription factor GATA2.99 Therefore, proper activation of Akt is required for normal adipogenesis and it could be speculated that Akt inhibition by the FKBP51-PHLPP could have a negative effect on this process."
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"Considering GSK3beta was found to be an important downstream molecule of PI3-K-Akt in our previous studies [XREF_BIBR] and that of others [XREF_BIBR], we reasoned that the activation of PI3-K, Akt, and GSK3beta complex signaling pathways played important role in mediating the LPS induced lung fibroblast proliferation, differentiation and collagen secretion."
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"Several studies have shown that the PI3K/Akt pathway can affect brain development and induce various neurological diseases by regulating neuronal cell proliferation and differentiation, autophagy and apoptosis, synaptic plasticity, and circuits (Hou and Klann 2004; Wu et al. 2020)."
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"Among the mentioned nanozymes, the cube enclosed by the (100) facet exhibits the highest CAT-like activity, causing it to provide superior protection to NPCs from oxidative stress induced by H 2 O 2 ; meanwhile, the octahedron enclosed by the (111) facet with the lowest CAT-like activity induces the most ROS production in ReNcell CX cells, which promotes neuronal differentiation by activated AKT/GSK-3β/β-catenin pathways."
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"Therefore, saponin fractions may have broad therapeutic efficacy against neurological diseases by re-inducing myelin formation.These pro-differentiation responses also appeared to be mediated by AKT and ERK signaling pathways (Fig. 2), consistent with previous studies implicating ERK1/2 and Akt/mTOR signaling individually in OL differentiation, initiation of myelination, and myelin membrane growth [36,52] as well as studies reporting mutual interactions between ERK1/2 and AKT/mTOR signaling in the regulation of OL differentiation [38]."
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"Activation of AKT pathway promotes cardiomyocyte differentiation through two different mechanisms, 1) through phosphorylation of GSK3beta to upregulate the expression levels of beta-catenin and Gata4; 2) through promotion of nuclear translocation of NF-kappaB by phosphorylating IKKbeta to inhibit cell apoptosis, which occurs due to increased Bcl2 expression."
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"Since recent studies pointed out the CSC subpopulation in tumours (including brain tumours) as the leading driver of malignant progression and relapse [XREF_BIBR] and previous results reported in this study clearly showed that PI3K and AKT downmodulation led to MDB cell growth inhibition, induction of cell death, and cellular differentiation, we examined the possible relationship between differentiation and cell death in MDB primary cells."
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"Therefore, puberty for young male subjects might represent the main therapeutic window for mitigating bone loss.We found that long-term SD decreased the phosphorylation of PI3K and AKT and inhibited the PI3K/AKT pathway in skeletal tissue in a possible way of explaining inhibited osteogenic differentiation and bone development."
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"In NSPCs, the elevating Akt activity in vitro increased cell survival and proliferation in cultured NSPCs derived from embryonic day 13 (E13) mouse cortex [XREF_BIBR], whereas Akt activation induced cell differentiation in cultured NSPCs derived from the medial ganglionic eminence (MGE) of E14 mouse [XREF_BIBR]."
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"KDR/Flk-1 is the high-affinity VEGF tyrosine kinase receptor on the cell membrane, it can be phosphorylated itself in response to VEGF stimulation and further transduce VEGF signal, downstream mitogen-activated protein kinase (MAPK), focal adhesion kinase (FAK) and protein kinase B (PKB) signaling pathways are then activated to regulate the migration, proliferation, and differentiation of angiogenesis-related cells [27,28]."
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"The induction of the PI3K pathway and thereby PDK1 and serine/threonine kinase protein kinase B (AKT) pathway, by CCR5, in turn, induces cell survival, glycolysis, cell proliferation, growth and proliferation of progenitor and stem cells, immune cell differentiation, and the release of eIF4E to promote cap dependent translation [XREF_BIBR, XREF_BIBR]."
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"Most of the studies on IGF-1R signaling have focused on its role in the differential activation of two important intracellular signaling pathways : the MAPK-ERK pathway, which regulates cell proliferation, differentiation, and tissue homeostasis, or the PI3K-AKT cascade, which promotes cell survival, metabolism, antiapoptosis, and differentiation."
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"Studies suggested that periostin could stimulate FAK and AKT phosphorylation via αv integrin, promote migration and differentiation of cardiac fibroblasts towards the infarcted region, and thereby avert cardiac rupture by enhancing the stiffness of the left ventricular wall through collagen synthesis (51)."
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"Thus, our results strongly suggest that complementarily to the known NRF2 activation, by repressing FOXO1, AKT induces erythroid differentiation of HE cells.Importantly, we showed here that FOXO1 repression induces a small-scale increase in the expression of non-oxidative PPP enzymes RPIA (ribose 5-phosphate isomerase A) and TKT (transketolase)."
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"Unexpectedly, the activation of PI3K/AKT was found to be required for ATRA to induce cell differentiation in AML cells, and PI3K/AKT activity elimination counteracted ATRA-induced AML cell differentiation without stimulating cell death, indicating that the simultaneous application of the PI3K/AKT inhibitor limited the maximal therapeutic effect of ATRA."
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"While the silencing miR-223 inhibits TGF- β1-induced expression of collagen I, collagen III, and a-SMA proteins, and the over-expression of miR-223 and downregulation of its target recombinant Ras GTPase activating protein 1 (RASA1) promote the phosphorylation of MEK1/2, ERK1/2, and AKT in cardiac fibroblasts, indicating that miR-223 can promote proliferation, migration, and differentiation of cardiac fibroblasts by down-regulating RASA1 expression and activating the renin-angiotensin system (RAS) signaling pathway, thereby aggravating cardiac fibrosis after MI (Liu et al., 2018a)."
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"Since a previous study has shown that Akt mediated inhibition of FoxO1 induces PPARgamma and subsequent adipocyte differentiation XREF_BIBR and PI3K is in the upstream of Akt signaling pathway, we further found that the protein levels of FoxO1 were increased in VAT (P < 0.0001, XREF_FIG)."
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"After FGF-FGFR binding, through the autophosphorylation of FGFRs, with the help of FGFR substrate 2 and PLCγ, signals are transferred to the RAS-ERK, PI3K/AKT, PKC, and JAK-STAT signaling cascades, which mediate the survival, proliferation, differentiation, or migration of cells (Inomata et al., 2015; Katoh, 2018)."
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"Figure 9 showed that icariin activates the PI3K/Akt signaling, and the activation of Akt led to UTX upregulation and EZH2 downregulation, resulting in the removement of H3K27me3 and eventually promoting osteogenic differentiation, keeping the balance of osteogenesis and adipogenesis, and preventing BMSC apoptosis."
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"Overexpression of Pref-1 activates MAPK and AKT signaling, which induces the differentiation of human pancreatic ductal cells into beta like cells with increased insulin synthesis and secretion, and improves glucose homeostasis by accelerating pancreatic ductal and beta cell regeneration after injury in a pancreatectomized diabetic animal model [XREF_BIBR]."
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"This suggests Akt3 may regulate T cells through alternative mechanisms, including potential negative feedback loops that attenuate PI3K activity and Akt phosphorylation,70 warranting further investigation.Our study clearly demonstrates that although both Akt1 and Akt2 signaling can induce CTL differentiation toward the effector stage and promote their effector functions, only Akt2 signaling enables CTLs to resist the immunosuppressive TME due to its ability to induce prompt cytotoxicity and suppress long-duration calcium influx."
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"Nonetheless, we here observed that the administration of S1P prohibits the activation of AKT-related signals in DPSCs under osteogenic differentiation conditions (Fig. 1) while the AKT activator SC79 prevents the S1P mediated reduction of these genes and attenuates the osteogenic differentiation of DPSCs (Fig. 4)."
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"BTK activity, together with tyrosine phosphorylation, triggers the action of protein kinase B (AKT) which in turn will mediate transcription factors for proliferation, differentiation, and signaling cascades for survival—RAS/RAF/MEK/ERK and PI3K/AKT/mTOR (Figure 2) [110,114,115,116,117]."
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"Complementary to our findings in P19 cells (Experiment 1), it was reported that active Akt can promote the differentiation of neuronal precursor cells into GABAergic neuron like cells XREF_BIBR and that phosphorylation of GABA A R via insulin induced Akt signalling can lead to an increase in the number of GABA receptors on the plasma membrane XREF_BIBR, thereby increasing inhibitory fast synaptic transmission in neurons."
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"Functional classification analysis of the 294 upregulated genes revealed significant enrichment in biological processes, such as cell differentiation, migration, proliferation, adhesion and chemotaxis, angiogenesis, cell death, and immune response, as well as Wnt, MAPK, PI3‐Akt, Hippo, and TGF‐beta pathways (Fig. 6A)."
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"Transgenic overexpression of an activated form of Akt, a downstream target of PI3K, in cartilage increased chondrocyte proliferation in the resting zone, and delayed hypertrophic differentiation in the growth plate, but promoted hypertrophic differentiation in craniobasal cartilaginous elements and vertebrae."
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"EXD also activates the Insulin-like growth factor 1 receptor/Phosphatidylinositol 3-kinase/Protein kinase B(IGF1/PI3K/AKT) signaling pathway by increasing serum IGF1 concentration and tibial Insulin-like growth factor 1 receptor(IGF1R), PI3K, and AKT expression, thereby promoting osteogenic differentiation and proliferation of osteoblasts."
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"Skurk et al. reported that beta-catenin-enhanced endothelial cell differentiation and migration are inhibited by PI3K and Akt inhibition, suggesting that Wnt and beta-catenin promotes angiogenesis and blood vessel growth via the induction of PI3-K and Akt signaling in endothelial cells [XREF_BIBR]."
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"Finally, inhibition of mTOR, PI3K or AKT blocked differentiation when applied at the start of the differentiation (10 days of treatment) but had less or no effect when applied from the half-way point (5 days of treatment) or just for the final 24 h, respectively (Fig. 4e and Extended Data Fig. 9d)."
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"Along with AMPK activation induced cell protective effects [XREF_BIBR], upon binding with Fstl1, Dip2a can upregulate AKT phosphorylation to protect cell from hypoxia and reoxygenation induced apoptosis and promote neovascularization by regulating endothelial cells ' migration and differentiation [XREF_BIBR]."
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"The induction of additional pathways by CCR5, include the PI-3 ' K pathway and thereby PDK1 and serine/threonine kinase protein kinase B (AKT), which in turn induces cell survival, glycolysis, cell proliferation, growth and proliferation of progenitor and stem cells, immune cell differentiation and the release of eIF4E to promote cap dependent translation (XREF_FIG)."