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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 24 Oct 2014.

CREB regulated transcription coactivator 1

mTORC1, TORC1, CRTC1, MECT1
Top mentioned proteins: mTOR, Akt, mTORC2, V1a, CAN
Papers using mTORC1 antibodies
Energetic communication between mitochondria and nucleus directed by catalyzed phosphotransfer.
Supplier
Hochman Shawn, In PLoS ONE, 2001
... To clone TORC1-GFP fusion protein expression construct, TORC1 coding sequence was amplified from pGEM-rTORC1 and inserted into pEGFP-N1 vector (Clontech) between HindIII and EcoRI ...
The biosynthesis of the subtilisin-related proprotein convertase PC3, but no that of the PC2 convertase, is regulated by glucose in parallel to proinsulin biosynthesis in rat pancreatic islets.
Supplier
Maedler Kathrin, In PLoS ONE, 1992
... INS-1E and islet extracts were used for analysis of mTORC1 signaling, protein biosynthesis, ER stress markers and ...
Papers on mTORC1
Activation of Glycogen Synthase Kinase 3β Ameliorates Diabetes-Induced Kidney Injury.
New
Kasinath et al., San Antonio, United States. In J Biol Chem, 22 Nov 2014
Studies in kidney proximal tubular epithelial cells showed that SNP abrogated HG-induced laminin increment by stimulating GSK3β and inhibiting Akt, mTORC1, and events in mRNA translation regulated by mTORC1 and Erk.
The combination of rapamycin and resveratrol blocks autophagy and induces apoptosis in breast cancer cells.
New
Holz et al., New York City, United States. In J Cell Biochem, 21 Nov 2014
UNLABELLED: Hyperactivation of the mechanistic target of rapamycin complex 1 (mTORC1) is a frequent event in breast cancer and current efforts are aimed at targeting the mTORC1 signaling pathway in combination with other targeted therapies.
Suppression of Feedback Loops Mediated by PI3K/mTOR Induces Multiple Overactivation of Compensatory Pathways: An Unintended Consequence Leading to Drug Resistance.
Review
New
Sinnet-Smith et al., Los Angeles, United States. In Mol Cancer Ther, 16 Nov 2014
However, mTORC1 and S6K also mediate potent negative feedback loops that attenuate signaling via insulin/insulin growth factor receptor and other tyrosine kinase receptors.
Let-7 Coordinately Suppresses Components of the Amino Acid Sensing Pathway to Repress mTORC1 and Induce Autophagy.
New
Impact
La Spada et al., San Diego, United States. In Cell Metab, 07 Nov 2014
Autophagy is regulated by the mTOR signaling pathway-the focal point for integration of metabolic information, with mTORC1 playing a central role in balancing biosynthesis and catabolism.
Branched-chain amino acids in metabolic signalling and insulin resistance.
Review
New
Adams et al., United States. In Nat Rev Endocrinol, 07 Nov 2014
A hypothesized mechanism linking increased levels of BCAAs and T2DM involves leucine-mediated activation of the mammalian target of rapamycin complex 1 (mTORC1), which results in uncoupling of insulin signalling at an early stage.
mTOR signalling, embryogenesis and the control of lung development.
Review
New
Walker et al., Saint Andrews, United Kingdom. In Semin Cell Dev Biol, 04 Nov 2014
UNLABELLED: The existence of a nutrient sensitive "autocatakinetic" regulator of embryonic tissue growth has been hypothesised since the early 20(th) century, beginning with pioneering work on the determinants of fetal size by the Australian physiologist, Thorburn Brailsford-Robertson. We now know that the mammalian target of rapamycin complexes (mTORC1 and 2) perform this essential function in all eukaryotic tissues by balancing nutrient and energy supply during the first stages of embryonic cleavage, the formation of embryonic stem cell layers and niches, the highly specified programmes of tissue growth during organogenesis and, at birth, paving the way for the first few breaths of life.
Sestrins Function as Guanine Nucleotide Dissociation Inhibitors for Rag GTPases to Control mTORC1 Signaling.
New
Impact
Li et al., New York City, United States. In Cell, 25 Oct 2014
Mechanistic target of rapamycin complex 1 (mTORC1) integrates diverse environmental signals to control cellular growth and organismal homeostasis.
Coordinated regulation of protein synthesis and degradation by mTORC1.
New
Impact
Manning et al., Boston, United States. In Nature, 18 Oct 2014
Mechanistic target of rapamycin complex 1 (mTORC1) promotes nutrient-consuming anabolic processes, such as protein synthesis.
The lysosomal v-ATPase-Ragulator complex is a common activator for AMPK and mTORC1, acting as a switch between catabolism and anabolism.
New
Impact
Lin et al., Xiamen, China. In Cell Metab, 02 Oct 2014
In this study we found, most surprisingly, that the late endosomal/lysosomal protein complex v-ATPase-Ragulator, essential for activation of mTORC1, is also required for AMPK activation.
Driving neural regeneration through the mammalian target of rapamycin.
Review
New
Maiese, Newark, United States. In Neural Regen Res, Sep 2014
mTOR is a component of the protein complexes mTOR Complex 1 (mTORC1) and mTOR Complex 2 (mTORC2) that are ubiquitous throughout the body and control multiple functions such as gene transcription, metabolism, cell survival, and cell senescence.
Metabolic reprogramming of stromal fibroblasts through p62-mTORC1 signaling promotes inflammation and tumorigenesis.
New
Impact
Moscat et al., Los Angeles, United States. In Cancer Cell, Aug 2014
The mechanism involves the regulation of cellular redox through an mTORC1/c-Myc pathway of stromal glucose and amino acid metabolism, resulting in increased stromal IL-6 production, which is required for tumor promotion in the epithelial compartment.
(R)-(+)-α-Lipoic acid protected NG108-15 cells against H2O2-induced cell death through PI3K-Akt/GSK-3β pathway and suppression of NF-κβ-cytokines.
New
Abdul Kadir et al., Kuala Lumpur, Malaysia. In Drug Des Devel Ther, Dec 2013
Moreover, pretreatment with R-LA stimulated the activation of PI3K-Akt through mTORC1 and mTORC2 components (mTOR, rictor and raptor) and production of antiinflammatory cytokine, IL-10 which led to the inactivation of glycogen synthase kinase-3β (GSK-3β) and reduction of both Bax/Bcl2 and Bax/Bcl-xL ratios, accompanied by inhibition of the cleaved caspase-3.
Increasing Superoxide Production and the Labile Iron Pool in Tumor Cells may Sensitize Them to Extracellular Ascorbate.
Review
New
Contreras et al., Tijuana, Mexico. In Front Oncol, Dec 2013
Measures which inhibit the constitutive hypoxia-inducible factor-1 (HIF-1) activity in cancers (such as salsalate and mTORC1 inhibitors, or an improvement of tumor oxygenation), or that inhibit the HIF-1-inducible pyruvate dehydrogenase kinase (such as dichloroacetate), can be expected to increase pyruvate oxidation.
mTORC1 Signaling in Oocytes Is Dispensable for the Survival of Primordial Follicles and for Female Fertility.
New
Shen et al., Göteborg, Sweden. In Plos One, Dec 2013
Mechanistic target of rapamycin complex 1 (mTORC1) is a central controller of cell growth and proliferation.
Reassessment of the Role of TSC, mTORC1 and MicroRNAs in Amino Acids-Meditated Translational Control of TOP mRNAs.
New
Meyuhas et al., Jerusalem, Israel. In Plos One, Dec 2013
Nonetheless, knockdown of raptor or rictor failed to suppress translational activation of TOP mRNAs by amino acids, suggesting that mTORC1 or mTORC2 plays a minor, if any, role in this mode of regulation.
Glutaminolysis activates Rag-mTORC1 signaling.
GeneRIF
Hall et al., Basel, Switzerland. In Mol Cell, 2012
We demonstrate that glutamine in combination with leucine activates mammalian TORC1 (mTORC1) by enhancing glutaminolysis and alpha-ketoglutarate production.
Activity-dependent transport of the transcriptional coactivator CRTC1 from synapse to nucleus.
Impact
GeneRIF
Martin et al., Los Angeles, United States. In Cell, 2012
Results indicate that synapse-to-nuclear transport of CRTC1 dynamically informs the nucleus about synaptic activity.
Attenuation of TORC1 signaling delays replicative and oncogenic RAS-induced senescence.
GeneRIF
Sun et al., Los Angeles, United States. In Cell Cycle, 2012
Inhibition of TORC1 retards, and to some extent reverses, phenotypic indicators of cellular senescence.
Phospholipase D and mTORC1: nutrients are what bring them together.
GeneRIF
Thomas et al., Cincinnati, United States. In Sci Signal, 2012
Studies indicate that phospholipase D (PLD) as a mediator of nutrients to mTORC1.
Chronic activation of mTOR complex 1 is sufficient to cause hepatocellular carcinoma in mice.
GeneRIF
Manning et al., Boston, United States. In Sci Signal, 2012
Data suggest that increased activation of mTORC1 can promote carcinogenesis.
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