Anagram & Information om | Engelska ordet MTOR


MTOR

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MTO
OR
TO
TOR

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37
MO
MOR
MOT
MR
MRO
MRT
MT


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Exempel på hur man kan använda MTOR i en mening

  • It is a mammalian target of rapamycin (mTOR) kinase inhibitor that reduces the sensitivity of T cells and B cells to interleukin-2 (IL-2), inhibiting their activity.
  • It is the 40-O-(2-hydroxyethyl) derivative of sirolimus and works similarly to sirolimus as an inhibitor of mammalian target of rapamycin (mTOR).
  • Key advances include the discovery that small molecules can function as “molecular glues” that promote protein–protein interactions, the co-discovery of mTOR and its role in nutrient-response signaling, the discovery of histone deacetylases and (with Michael Grunstein and David Allis) the demonstration that chromatin marks regulate gene expression, the development and application of diversity-oriented synthesis to microbial therapeutics, and the discovery of vulnerabilities of cancer cells linked to genetic, lineage and cell-state features, including ferroptotic vulnerabilities.
  • The mutations disregulated mTOR, the protein inhibited by everolimus, allowing it to reproduce without limit.
  • Laboratory studies attribute these apparent effects to inhibition of mTOR, inhibition of complex I, with phenformin being a more potent inhibitor than metformin,.
  • ARID1A loss activates annexin A1 expression, which is required for drug resistance (mTOR inhibitor or trastuzumab) through its activation of AKT.
  • Known effects include decrease of expression of effectors in the mTOR pathway, and suppression of cyclin D1 and PARP-1.
  • The physiological consequences of mTOR inhibition following endomembrane damage are many including induction of autophagy and metabolic switching.
  • When the kinase activity of mTOR is activated, its downstream effectors, the synthesis of cell cycle proteins such as cyclin D and hypoxia-inducible factor-1a (HIF-1a) are increased.
  • MAPKAPK2 mediates the initiation of the senescence-associated secretory phenotype (SASP) by mTOR (mechanistic target of rapamycin).
  • Ataxia telangiectasia mutated (ATM) is a kinase that (similar to mTOR) can phosphorylate KAP1 resulting in the switch from viral latency to the lytic cycle.
  • It upregulates S6 kinase, the downstream effector ribosomal protein, and it downregulates the mTOR kinase.
  • In particular, upregulation of HIF-1 in response to hypoxia upregulates DDIT4, leading to activation of Tsc1/2 via 14–3–3 shuttling and subsequent downregulation of mTOR via Rheb.
  • The frequent overactivation of mTOR (mammalian target of rapamycin) signaling has also been observed in epithelioid sarcoma.
  • In hepatocellular carcinoma, osteosarcoma, lung adenocarcinoma, and muscle-invasive bladder cancer, overexpression of BZW2 lead to overactivation of the AKT/mTOR signaling pathway by increasing phosphorylation of AKT and mTOR.
  • Upon this signalization it causes inhibition of components of NF-κB pathway, kinases mTOR, TAK1, FYN, p38, JNK, ERK and it also causes activation of phosphatase PTEN, kinase MER, transcription factor STAT3 and adaptor protein p62 (DOK1).
  • Ridaforolimus (also known as AP23573 and MK-8669; formerly known as deforolimus) is an investigational targeted and small-molecule inhibitor of the protein mTOR, a protein that acts as a central regulator of protein synthesis, cell proliferation, cell cycle progression and cell survival, integrating signals from proteins, such as PI3K, AKT and PTEN known to be important to malignancy.
  • Also, leptin has been shown to activate signal transduction pathways associated with dopamine and mTOR, which can increase synaptogenesis.
  • The Sestrins constitute a family of evolutionarily-conserved stress-inducible proteins that suppress oxidative stress and regulate adenosine monophosphate-dependent protein kinase (AMPK)-mammalian target of rapamycin (mTOR) signaling.
  • p53 activation has also been implicated as a necessary mechanism for the development of TNTs, as the downstream genes up-regulated by p53 (namely EGFR, Akt, PI3K, and mTOR) were found to be involved in nanotube formation following hydrogen peroxide treatment and serum starvation.


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