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IL1B activates AKT. 110 / 113
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"IL-1β was shown to activate MAPKs and AKT ( Chen et al., 2007 )."
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"Exogenous expression of either SHPS-1 mutants that lack SHP-2 binding function or a dominant negative mutant of SHP-2 markedly inhibited the activation of Erk 1/2 and Akt by IL-1beta, whereas wild type SHPS-1 did not."
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"Of note, IL-1β activated Akt to less extent and for shorter term than TNF-α."
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"Its anti-inflammatory activity is mediated by modulation of interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α), prostaglandin E (PGE ), and nitric oxide by suppressing the phosphoinositide-3-kinase (PI3K)/protein kinase B (Akt)/nuclear factor kappa light chain enhancer of the activated B cell (NF-κB) signaling pathway."
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"Davis and others have confirmed that IL-1β can activate Akt when stimulating hypothalamus neurons, and that activation relies on recruiting the subunits of PI3K-p85 to the IL-1RI of neuron membranes ([MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Previous studies have shown that TNF-α and IL-1β activate the PI3K/Akt, NF-κB, MAPK/Erk and STAT3 signaling pathways in different cell types [23–26]."
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"Interestingly we found the inhibitory effects of melatonin on IL-1β-induced activation of ERK, p38, Akt and TAK1 in this study."
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"These results showed that the PI3K and Akt signaling pathway is activated by DEP stimulation, further up-regulating IL-8 and IL-1beta expression."
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"3.5 Arctigenin inhibited the PI3K and Akt signalling pathway induced by IL-1beta in human OA chondrocytes."
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"Specifically, IL-1β activated AKT kinase, and expression of activated AKT led to the reduction of cGAMP production."
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"IL-1β (10 ng/ml) administration increased the ratio of p-PI3K/PI3K and p-AKT/AKT in a time-dependent manner between 30 min and 1 h compared with that in controls (Fig. 6G, H)."
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"In our previous study [XREF_BIBR], IL-1beta stimulated Akt activation in DOK and OSCC cells, thus facilitating a negative feedback regulation mechanism."
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"It might be due to the fact that IL-1β activated Akt to less extent and for shorter term than TNF-α, as shown in this report ( Fig. 4 D)."
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"Using U73122 in Balb 3T3 fibroblasts, Amin et al. [ xref ] showed that the PLC-PKC signaling cascade involving PLC-γ was required for IL-1β-induced Akt activation."
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"For instance, it was found that metformin decreases interleukin 1 beta (IL-1beta) induced activation of proinflammatory phosphokinases Akt (protein kinase B), p38 (mitogen activated protein kinase)."
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"In the current study, IL-1β did not induce significant VEGFR2 phosphorylation or Akt activation, and it induced only minimal GSK3β phosphorylation."
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"Also, qPCR exhibited that by inhibiting HMGB1, RAGE, and PI3K/Akt pathways, the mRNA levels of iNOS, IL-1β and TNF-α were significantly reduced, and the mRNA expression of IL-4, IL-10 and Arg-1 were varyingly upregulated (Fig. 5B)."
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"A number of studies have confirmed that the NF-κB signaling pathway and AKT pathway induced by IL-1β are also involved in the pathogenesis of KBD (Cao et al., 2008; Yan et al., 2010; Tang et al., 2012; Huimin Wang et al., 2014; Zhou et al., 2014), indicating that there are similarities between KBD and the pathological process of osteochondropathies regulated by cyclins and CDKs."
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"Then, NLRP3 inflammasome activation can promote the release of IL-1beta from macrophages, and activated IL-1beta can activate c-Jun N-terminal kinase (JNK), IkappaB kinase (IKK), and the IRS-1 / PI3K and Akt axis via the IL-1 receptor (IL-1R)."
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"The results clearly show that IL-1beta induced Akt activation in a time dependent manner; PDGF-bb or IGF-1 inhibited this process (XREF_FIG)."
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"IL-1β activates Akt through a PI3K-dependent manner. xref , xref Akt is a serine/threonine kinase that is known to promote cell survival. xref Therefore, we investigated whether IL-1β could affect the Akt pathway and whether PKDi could impair IL-1β-mediated signaling, leading to Akt activation in chondrocytes."
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"It was further noted that reduced IL-1beta production also inhibited UUO induced PI3K and AKT signaling, and both of which ultimately protected mice from UUO induced renal fibrosis."
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"Extracellular Hmgb1 thus bound to TLR4, and by which, it activated MyD88-NFkappaB pathway to enhance IL-1beta expression, which in turn promoted TGF-beta/Smad2/3 and Pi3k and Akt signaling to exacerbate renal fibrosis."
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"IL-1β increased Akt activation by about 1.8-fold after 30 min of incubation and maintained this stimulation up to 1 h. Thereafter, phosphorylation decreased sharply (Figure 8A)."
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"XREF_BIBR, XREF_BIBR Of note, other than stimulating TGF-beta1 secretion, there is also evidence indicating that IL-1beta can activate PI3K and Akt signaling, 27 and thereby enhancing renal fibrosis."
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"35 In the previous study, it was reported that IL-1beta induces IGF-1 upregulation and Akt activation, 13 which play important roles in adaptive cardiac hypertrophy."
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"The activation of Akt, PI3K, nuclear factor (NF)-kappaB, Erk, Jnk, and p38 kinase by IL-1beta and TNF-alpha was diminished with CHIR 99021 in GO cells."
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"We found that LY294002 pretreatment largely blunted IL-1β-induced activation of AKT and phosphorylation of NF-kB signaling components including IκBα and p65 ( Fig. 7 D and E)."
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"In contrast, metformin has been reported to suppress IL-1β-induced activation of Akt but does not affect PI3K activity in smooth muscle cells [9] ."
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"As shown in Fig. 4K, the expressions of IL-1β and IL-6 in HCECs were reduced by ebselen.3.7 Ebselen inhibited A. fumigatus-induced phosphorylation of p38 MAPK and activated the PI3K/Akt and Nrf2/HO-1 signaling pathways."
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"The results showed that IL-1β increased the ratio of p-AKT/AKT and p-mTOR/mTOR, and OMT inhibited this increase."
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"Similarly, Lee et al. (2020) demonstrated that Candida spp., when co-cultured with Fusobacterium nucleatum, enhanced IL-1β secretion, activating the PI3K/Akt pathway and worsening tumour-promoting inflammation [36]."
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"Cell experiments revealed that wogonin reduced M5-induced HaCaT cell viability and TNF-α and IL-1β expressions by blocking the PI3K/AKT pathway in a dose-dependent manner."
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"It has been reported that IL-1β enhances the Akt/mTOR metabolic signaling pathway in CD4 + T cells ( Wyszynski et al., 2016 )."
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"13 Thus, IL-1beta upregulation may be a key process in TLR2 mediated cardiac adaptive response to pressure overload, although the mechanisms in which the TLR2 and IL-1beta axis induces IGF-1 upregulation and Akt activation remain nonelucidated."
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"Results suggested that activation of PI3K and Akt signaling pathway stimulated by IL-1beta with or without additional resveratrol was significantly inhibited."
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"According to the work done by Madrid et al. [28] , in the context of IL-1β-induced Akt activation, treatment of cells with IL-1β or expression of myr-Akt enhanced the phosphorylation and activation o[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"IL-1beta induces phosphorilation of Akt and activation of PI3K and AKT XREF_BIBR - XREF_BIBR and intravitreal injections of this cytokine rescued axotomized RGC from retrograde cell death XREF_BIBR."
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"However, the effects of IL-1beta on Monocyte Chemotactic Factor-1 (MCP-1) of dental pulp cells and its relation to transforming growth factor beta activated kinase-1 (TAK1), PI3K and Akt, and MEK and ERK signaling and COX activation are not fully clear."
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"Its anti-inflammatory activity is mediated by modulation of interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α), prostaglandin E (PGE ), and nitric oxide by suppressing the phosphoinositide-3-kinase (PI3K)/protein kinase B (Akt)/nuclear factor kappa light chain enhancer of the activated B cell (NF-κB) signaling pathway."
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"We found that short-term IL-1beta and TNF-alpha treatment not only activated pro inflammatory pathways involving phosphorylation of JNK, IKKalpha, and p38MAPKalpha, but also induced strong transient a[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Trans-cinnamaldehyde inhibited the inflammation induced by IL-1β in chondrocytes through the PI3K/AKT pathway, which suggests that TCA might serve as a potential therapeutic agent for osteoarthritis treatment."
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"IL-1beta activated the AKT pathway (XREF_FIG), ERK pathway (XREF_FIG), JNK pathway (XREF_FIG) and nuclear factor-kappaB (NF-kappaB) pathway (XREF_FIG)."
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"On the other hand, IL-1beta activates PKB, which induces proliferation."
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"Of note, IL-1β activated Akt to less extent and for shorter term than TNF-α."
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"Therefore, we examined whether LDR modulates IL-1beta-induced Akt activity and found that LDR at both 0.5 and 1 cGy suppressed Akt activation induced by IL-1beta in chondrocytes (XREF_FIG E)."
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"Moreover, IL-1β and IL-6 secretion from myeloid cells stimulate phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathways, which, in turn, activat[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Using WB, we revealed that IL-1β significantly activated the PI3K/AKT signalling pathway, and the ratio of p-PI3K/PI3K and p-AKT/AKT was significantly increased compared with the control group."
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"Western blotting results displayed that NF-κB, PI3K/Akt and MAPK pathways were significantly induced by IL-1β, 4μ8C suppressed the phosphorylation NF-κB p65, p38 and JNK markedly, it also partly inhib[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"At the same time, IL-1beta is able to activate PKB via a different set of kinases such as JNK or p38MAPK, which results in induction of proliferation."
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"It might be due to the fact that IL-1β activated Akt to less extent and for shorter term than TNF-α, as shown in this report ( Fig. 4 D)."
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"Furthermore, the pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) were found to be upregulated, which can cause AKT and mTOR deregulation and subsequent tumor progression [ 180 ]."
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"Given that IL-1β-induced production of various inflammatory mediators and cartilage-degrading factors reportedly activated Akt through a PI3K-dependent manner, we therefore investigated whether CLU could impair activation of PI3K/Akt pathway induced by IL-1β in knee OA FLSs."
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"Actually, one of the key actions of IL-1beta is to activate Akt signaling; based on the canonical Wnt pathway, inactivation of the serine/threonine kinase GSK3 by Akt increases beta-catenin accumulation and expression of Tcf/Lef target genes."
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"We demonstrated evidence that loss of Chop represses Hmgb1 and TLR4 signaling following UUO induction, leading to repressed NFkappaB transcriptional activity along with suppressed IL-1beta production, which then reduces TGF-beta1 production and Pi3K and Akt activity to attenuate the development of renal fibrosis."
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"It should be noted that the tangeretin suppresses IL-1β-induced Akt activation in human lung carcinoma cells ( xref )."
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"Furthermore, IL-1beta activated the PI3K and Akt signaling via enhancing the phosphorylation of Akt at S473 and T308."
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"Some studies indicated that IL-1beta can trigger the activation of both Akt pathway and NF-kappaB pathway, which appears to be important molecular links between inflammation and tumor [XREF_BIBR, XREF_BIBR]."
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"In human embryonic kidney 293 cells, IL-1beta induces IkappaB kinase beta (IKKbeta) activation, IkappaBalpha degradation, NF-kappaB transactivation, and weak Akt activation."
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"In recent years, many studies showed that IL-1beta can activate the PI3K and Akt after binding with its receptors; it was found that IL-1beta can activate PI3K in endothelial cells, glial cells of rats and retinal ganglion cells [24] then, PI3K leads to Akt phosphorylation, which further affects its downstream molecules by adjusting mTORC1, and further makes its downstream Akt phosphorylation and its activation [23]."
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"More detailed signaling pathways regulatory mechanisms into V. alginolyticus induced inflammatory response in mice need to be explored and are warranted in the future.In summary, V. alginolyticus regu[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Davis and others have confirmed that IL-1β can activate Akt when stimulating hypothalamus neurons, and that activation relies on recruiting the subunits of PI3K-p85 to the IL-1RI of neuron membranes ([MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"In the brain inflammation of mice induced by LPS, salidroside (50 mg/kg) can reduce neutrophil infiltration and inhibit the expression of NF-κB, TNF-α, and IL-1β by activating the PI3K/Akt pathway, thus playing an anti-inflammatory role [152]."
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"Research by Chen et al. indicated that salidroside downregulates the expression levels of TNF-α, TGF-β1, IL-1β, and Bax, and upregulates Bcl-2, VEGF, Akt, and eNOS, exerting anti-inflammatory effects and alleviating myocardial fibrosis and remodeling after myocardial infarction (Chen et al., 2019)."
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"Inflammasome activation in Jak2 macrophages increased secretion of IL-1β, which increased AKT and ERK signaling and thereby led to both increased proliferation and pyroptotic cell death (Fig. 2b)."
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"One study showed that the increase of FASN-mediated lipid synthesis of macrophages could enhance the caspase-1 activation mediated by NLRP3 and IL-1β expression through Akt and P38 MAPK pathways 125."
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"IL-1beta, COX-2-dependent PGE 2 activated the PI3-K and AKT and p38 signaling pathways, which were in turn responsible for MMP-1 synthesis via NF-kappaB- and c-Jun-transactivating pathways."
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"Addition of 1 ng/ml IL-1beta activated both p42 and p44 MAPK as well as AKT."
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"The underlying mechanism related to HAS gene suppression is not entirely clear, but our study revealed that ibrutinib attenuated IL-1β-induced Akt and MAPK activation, and this may have inhibited IL-1β induced HAS1,2 and 3 transcription."
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"IL-1β differentially activates various signaling molecules such as MEK/ERK, p38, PI3K/Akt, NF-kB, and possibly TAK1 in HDPCs [7,8,36]."
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"IFNγ (158%) and IL-1β (141%) significantly increased Akt activity."
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"FGF23 enhances IL-1β expression by activating the PI3K, Akt, and NF-κB pathways."
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"The phosphorylation levels of PI3K, AKT, and mTOR were suppressed after SIRT3 overexpression, while siRNA-mediated SIRT3 knockdown significantly enhanced the activation of PI3K, AKT, and mTOR induced by IL-1β stimulation."
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"Our recent study further demonstrated that monomeric/fibrillar collagens and PDGF-BB/IL-1β stimuli can converge on p66Shc to modulate SMC cycle and proliferation through phosphatidylinositol 3-kinase [MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"YU [31] found that when gouty arthritis occurs, it stimulated the synthesis and release of IL-1β, which eventually activated AKT."
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"These results showed that IL-1beta activated the p38 and MAPK and PI3K and Akt signaling pathways, while IL-1R1 antibody significantly reduced the p38 and MAPK and PI3K and Akt signaling as compared to the IL-1beta treated group (XREF_FIG)."
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"SalB inhibits the transcription of pro-collagen genes CoI and CoⅢ, and the expression of CTGF, IL-1β, and IL-6 by modulating the AKT, MAPK/ERK, and TGF-β/Smad signaling pathways (Dai et al., 2015a)."
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"These western blot results showed that IL-1beta enhanced the activation of the p38 and MAPK and PI3K and Akt in breast cancer cells, and the addition of the inhibitors detained the stimulation."
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"These results indicate that the p38 and MAPK and PI3K and Akt signaling pathways activated by IL-1beta play a critical role in these morphological changes, leading to VM responses."
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"To further exacerbate injury caused by ischemia, IL-1β modulates the PI3K/AKT pathway, promotes IL-6 and other cytokines, and operates synergistically in the ischemic region (167)."
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"IL-1beta activated the MAPK ( ERK , JNK , and p38 ) , AKT , and NF-kappaB signaling pathways within 48 hours of treatment ( Fig. S4A ) ."
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"IL-1beta was found to stimulate MMP-9 synthesis and release by activating PI3K-Akt and MEK1-ERK signaling cascades, while p38 signaling was not involved [XREF_BIBR]."
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"As shown in xref row I , IL-1β induced activation of Akt in a time-dependent manner."
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"As shown in XREF_FIG row I, IL-1beta induced activation of Akt in a time dependent manner."
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"To examine the 4-MU effect on phosphorylation of NF-kappaB and AKT, early signaling events during interleukin (IL)-1beta treatment of anterior cruciate ligament (ACL)-derived cells, the peak time-point of NF-kB and PI3K and AKT phosphorylation in cells treated with IL-1 beta."
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"In addition, β-catenin can also be activated via adenomatous polyposis coli (APC)-independent pathways, such as nuclear factor κB (NF-κB) or AKT pathway induced by tumor necrosis factor alpha (TNF-α),[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"IL-1b also stimulates transactivation of growth factor receptors and PI3K and Akt, leading to the expression of inflammatory proteins."
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"As shown in Figure 4A and B, IL-1β significantly activated PI3K, AKT, and mTOR, while the increased phosphorylation levels of PI3K, AKT, and mTOR were inhibited with the pretreatment with different concentrations of CRA."
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"As shown in xref and B, IL-1β significantly activated PI3K, AKT, and mTOR, while the increased phosphorylation levels of PI3K, AKT, and mTOR were inhibited with the pretreatment with different concentrations of CRA."
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"These data suggested that IL-1β stimulated transactivation of EGFR/Akt cascade via c-Src-dependent manner in bMECs."
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"IL-1beta rapidly activated Akt and ERK."
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"It was confirmed that the expression of phosphorylated MAPK, AKT, and NF-κB activated by IL-1β decreased when treated with EA, uRO-w, and UA."
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"IL-1beta also activates the PI3K and AKT axis (XREF_SUPPLEMENTARY G) and MAPKs (XREF_SUPPLEMENTARY H-S2J), in addition to several other aforementioned transcription factors."
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"Free radicals and reactive oxygen species (particularly H2O2), cytokines (IL1beta, IL-2, IL-17, IL-18, TNF-alpha), UV light, pathogenic bacteria and viruses, which activate the kinases, MAPKs (mitogen activated protein kinases), protein kinase Akt and the complex of IkappaB kinase, catalyzing phosphorylation, ubiquitination and proteolysis of IkappaB proteins, are involved in the activation of NF-kappaB."
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"IL-1beta promotes esophageal squamous cell carcinoma growth and metastasis through FOXO3A by activating the PI3K/AKT pathway."
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"LPS, IL-1beta, and TNF-alpha, which mediate ocular inflammation, stimulate activation of p38, ERK, and Akt kinases in the corneal cell line."
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"As shown in Fig. 5 , I, IL-1β-induced activation of Akt in a time-dependent manner."
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"Effect of IGF-1 or/and PDGF-bb on IL-1β-induced activation of Akt in chondrocytes in monolayer cultures."
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"We examined the activation of MAPK and Akt signal proteins by western blot and determined that IL-1beta activated all three MAPKs (ERK, p38, and JNK) and Akt."
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"The results clearly show that IL-1β induced Akt activation in a time-dependent manner; PDGF-bb or IGF-1 inhibited this process ( xref )."
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"The activation of AKT and NF-κB by IL-1β was markedly inhibited by CAPE, whereas the activity of mitogen-activated protein kinases (MAPKs) was not affected."
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"Therefore, we determined IL-1α expression but not IL-1β expression in the HaCaT cells.Previous studies showed that, stimulating HaCaT cells with hexavalent chromium, a typical contact sensitizer, coul[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"LPS and IL-1beta induced phosphoylation of Akt at T308 in Traf6 +/+ MEFs in the presence of 10% FBS; this effect was reduced in Traf6 -/- MEFs (XREF_SUPPLEMENTARY)."
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"Riera et al confirmed that IL-1β activates the PI3K/PKB pathway to upregulate glucose transport in Sertoli cells [ 57 ]."
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"This mechanism involves the activation of phosphatases and the inhibition of IL-1β-induced activation of NF-κB and protein kinase B (AKT) ( xref )."
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"A dominant negative mutant (Mal-P/H) of MyD88 adapter like protein (Mal), a protein with homology to MyD88, failed to inhibit LPS- or IL-1 beta induced Akt activity."
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"APOD blocked activation of the PI3K/ AKT/mTOR signaling pathway induced by IL-1β in chondrocytes."
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"What’s more, AKT/P65 pathway was activated by IL-1β to promoted HIF-2α expression and B cells induced HIF-2α upregulation activated DLL4 to initiate DLL4/Notch1 signals."
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"Although the observed changes were not as pronounced as those observed in the absence of Rab8a, the absence of Rab8b resulted in decreased Akt activation, decreased mRNA levels for the anti-inflammatory cytokine IL-10, and increased levels for the pro-inflammatory cytokines IL-1β and Tnfα after S. Typhimurium infection (Fig. 2c and Extended Data Fig. 3)."
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"The experimental results show that curcumin could down-regulate the expression of NF-κB targets including COX-2 and MMP-9 and inhibit IL-1β induced stimulation of upstream protein kinase B Akt."
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