Akt scaffold proteins: the key to controlling specificity of Akt signaling

Bao, Fan; Hao, Peiqi; An, Su; Yang, Yang; Liu, Ying; Hao, Qian; Ejaz, Mubashir; Guo, Xuewu; Xu, Tian‐Rui

doi:10.1152/ajpcell.00146.2020

Cited by 10 publications

(8 citation statements)

References 123 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Therefore, the activity of Akt and mTOR were analyzed in the tail tissues at day 0, 3, 7 and 14 after injury in the low and normal temperature groups. The Akt activity is indicated by phosphorylation of Thr308 and Ser473 27 . Our results revealed that Akt activation level in the normal temperature (28 °C) group was significantly augmented at the beginning stage of regeneration.…”

Section: Resultsmentioning

confidence: 99%

Akt/mTOR integrate energy metabolism with Wnt signal to influence wound epithelium growth in Gekko Japonicus

et al. 2022

View full text Add to dashboard Cite

The formation of wound epithelium initiates regeneration of amputated tail in Gekko japonicus. Energy metabolism is indispensable for the growth of living creatures and typically influenced by temperature. In this study, we reveal that low temperature lowers energy metabolism level and inhibits the regeneration of amputated tails of Gekko japonicus. We further find that low temperature attenuates the activation of protein kinase B (Akt) and mammalian target of rapamycin (mTOR) in regenerated tissues upon injury signals, and the inhibition of Akt hinders proliferation of the wound epithelium. Additionally, wingless/integrated (Wnt) inhibition suppresses epithelium proliferation and formation by inhibiting Akt activation. Finally, low temperature elevates the activity of adenylate-activated kinase (AMPK) pathway and in turn attenuates wound epithelium formation. Meanwhile, either mTOR downregulation or AMPK upregulation is associated with worse wound epithelium formation. Summarily, low temperature restricts wound epithelium formation by influencing energy sensory pathways including Akt/mTOR and AMPK signaling, which is also modulated by injury induced Wnt signal. Our results provide a mechanism that incorporates the injury signals with metabolic pathway to facilitate regeneration.

show abstract

Section: Resultsmentioning

confidence: 99%

Akt/mTOR integrate energy metabolism with Wnt signal to influence wound epithelium growth in Gekko Japonicus

et al. 2022

View full text Add to dashboard Cite

show abstract

“…AKT, as a serine/threonine protein kinase, is a central effector molecule of the phosphoinositide 3-kinases/protein kinase B (PI3K/AKT) signaling pathway with its location at its hub [ 26 ]. AKT can influence downstream mTOR signaling, thereby contributing to the PI3K/AKT/mTOR pathway.…”

Section: Discussionmentioning

confidence: 99%

Effects on Autophagy of Moxibustion at Governor Vessel Acupoints in APP/PS1double-Transgenic Alzheimer’s Disease Mice through the lncRNA Six3os1/miR-511-3p/AKT3 Molecular Axis

Jia

Zhu

She

et al. 2022

Evidence-Based Complementary and Alternative Medicine

View full text Add to dashboard Cite

Objective. To explore the effect and mechanism of moxibustion at acupoints of the governor vessel on lncRNA Six3os1 in amyloid precursor protein/presenilin1 (APP/PS1) double-transgenic Alzheimer’s disease (AD) mice. Methods. Twenty-four specific pathogen-free and APP/PS1 double-transgenic male mice were randomly allocated into the AD model and moxibustion groups, with 12 cases in each group. Twelve syngeneic C57BL/6J mice were selected as the control group. Mice in the moxibustion group received aconite cake-separated moxibustion at the Baihui acupoint. Suspension moxibustion was applied at Fengfu and Dazhui for 15 minutes each day. All treatments were conducted over two weeks. Control and AD model mice were routinely fed without any intervention. Behavioral observation tests were conducted before and after the intervention. The autophagosome in the hippocampus was observed using transmission electron microscopy. Immunohistochemistry was performed to detect Aβ1-42 expression. LC3B and P62 expressions were evaluated by immunofluorescence. The expression levels of the lncRNAs Six3os1, miR-511-3p, and AKT3 were detected by qRT-PCR. The differential expression of PI-3K, AKT3, mTOR, LC3B-II/I, and P62 proteins in the hippocampus was detected by western blot. The dual-luciferase assay was undertaken to examine the targeting relationships of the lncRNAs Six3os1, miR-511-3p, and AKT3. Results. Compared with the control group, the AD model showed higher escape latency in the Morris Water Maze and reduced autophagic vacuoles in the cytoplasm of hippocampal neurons (both p < 0.01 ). Compared with the control group, the AD model showed higher expression of Aβ1-42, the lncRNAs Six3os1, PI-3K, mTOR, P62, and AKT3 protein (all p < 0.01 ); but lower mir-511-3p and LC3B (both p < 0.01 ). Compared with the AD model group, the moxibustion group had a shorter escape latency, more autophagic bubbles in the hippocampus, and lower expression of positive Aβ1-42, the lncRNAs Six3os1, PI-3K, mTOR, P62, and AKT3 protein (all p < 0.01 ). In contrast, the levels of miR-511-3p and LC3B proteins were considerably increased in the moxibustion group compared to the AD model group (both p < 0.01 ). Based on the dual-luciferase assay, there was a targeting link among the lncRNAs Six3os1, miR-511-3p, and AKT3. Conclusion. Moxibustion at acupoints of the governor vessel can suppress the lncRNA Six3os1 expression, promote cell autophagy, accelerate Aβ1-42 clearance and alleviate cognitive dysfunction of AD mediated by the PI3K/AKT/mTOR signaling pathway through the lncRNA Six3os1/miR-511-3p/AKT3 axis.

show abstract

“…The AKT signaling pathway is required for HADH to regulate cell proliferation, migration, and invasion, according to Shen et al (Shen et al, 2017). AKT signaling is a growthregulating biological pathway that has been shown to improve tumor cell survival, proliferation, and motility in a variety of tumor types (Chan et al, 2014;Bao et al, 2021;Junaid et al, 2021;Tsai et al, 2021). AKT, also known as protein kinase B (PKB), is a critical node in many signaling pathways, as well as one of the most essential and flexible protein kinases in human physiology and illness (Meier and Hemmings, 1999;Manning and Cantley, 2007;Revathidevi and Munirajan, 2019).…”

Section: Gastric Cancer 211 Functional Characteristics and Clinical F...mentioning

confidence: 99%

Short-chain L-3-hydroxyacyl-CoA dehydrogenase: A novel vital oncogene or tumor suppressor gene in cancers

Zhang

et al. 2022

Front. Pharmacol.

View full text Add to dashboard Cite

The reprogramming of cellular metabolism is frequently linked to tumorigenesis. Glucose, fatty acids, and amino acids are the specific substrates involved in how an organism maintains metabolic equilibrium. The HADH gene codes for the short-chain L-3-hydroxyacyl-CoA dehydrogenase (HADH), a crucial enzyme in fatty acid oxidation that catalyzes the third phase of fatty acid oxidation in mitochondria. Increasing data suggest that HADH is differentially expressed in various types of malignancies and is linked to cancer development and progression. The significance of HADH expression in tumors and its potential mechanisms of action in the onset and progression of certain cancers are summarized in this article. The possible roles of HADH as a target and/or biomarker for the detection and treatment of various malignancies is also described here.

show abstract

Akt scaffold proteins: the key to controlling specificity of Akt signaling

Cited by 10 publications

References 123 publications

Akt/mTOR integrate energy metabolism with Wnt signal to influence wound epithelium growth in Gekko Japonicus

Akt/mTOR integrate energy metabolism with Wnt signal to influence wound epithelium growth in Gekko Japonicus

Effects on Autophagy of Moxibustion at Governor Vessel Acupoints in APP/PS1double-Transgenic Alzheimer’s Disease Mice through the lncRNA Six3os1/miR-511-3p/AKT3 Molecular Axis

Short-chain L-3-hydroxyacyl-CoA dehydrogenase: A novel vital oncogene or tumor suppressor gene in cancers

Contact Info

Product

Resources

About