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What causes Rett Syndrome
Published in Rosa Angela Fabio, Tindara Caprì, Gabriella Martino, Understanding Rett Syndrome, 2019
Rosa Angela Fabio, Tindara Caprì, Gabriella Martino
At a nuclear level, it has been proposed that MeCP2 compacts chromatin structure and represses transcription by recruiting, as in a bridge model, the nuclear receptor co-repressor–silencing mediator of retinoic acid and thyroid hormone receptor (NCOR–SMRT) co-repressor complex, or activates transcription by recruiting the co-activator cyclic AMP-responsive elementbinding protein 1 (CREB1) (Lyst et al., 2013; Nan et al., 1997).
Neuropsychology of Cognitive Aging in Rodents
Published in David R. Riddle, Brain Aging, 2007
Joshua S. Rodefer, Mark G. Baxter
Brightwell and colleagues [39] investigated the effectiveness of signal transduction in aged rats with impaired spatial performance. Individual proteins from the CREB family can function as either enhancers (e.g., CREB1) or repressors (e.g., CREB2) and influence the short-term to long-term memory transitions. Aged animals that were impaired in the Morris water maze were found to have lower levels of CREB1 in the hippocampus compared to both younger animals and aged non-impaired animals, suggesting dysregulation of CREB1 levels may lead to some aspects of spatial learning deficits in aged subjects. Aged rats with impaired spatial memory, compared to young rats, demonstrated increased protein kinase C (PKC)-gamma immunoreactivity in the CA1 region of the hippocampus, but not in the dentate gyrus [40]. Furthermore, this increased PKC-gamma activity in CA1 was significantly correlated with spatial memory deficits. These data are consistent with a report that demonstrated a significant relationship between choice accuracy and PKC-gamma immunogenicity in the hippocampal CA1 region, but not amygdala, of aged animals [41].
Ca2+/calmodulin-dependent protein kinase IV attenuates inflammation and mitochondrial dysfunction under insulin resistance in C2C12 cells
Published in Archives of Physiology and Biochemistry, 2023
CREB has been identified as a constitutive transcription factor that contains both activator (CREB1) and repressor (CREB2) (Kandel 2012). CREB1 is widely expressed and plays a significant role in neuronal activity, memory, synaptic plasticity, metabolism, and behaviours, its functions were primarily regulated by extracellular regulated protein (ERK), protein kinase B (PKB/Akt), cAMP‐dependent protein kinase A (PKA) and Ca2+/calmodulin‐dependent protein kinases (CaMKs) (Bartsch et al.1998). CaMKIV as a major upstream regulator which could phosphorylate CREB1 at Ser133 by inducing intracellular Ca2+ increase (Matthews et al.1994). Therefore, we speculated that the protective effect of CaMKIV in present of this study probably through the activation of CREB1. Our results first demonstrated CaMKIV treatment increased phosphorylation of CREB1 expression in C2C12 cells. Moreover, the protective effects of CaMKIV on mitochondrial function, insulin signalling, and inflammatory response were nullified by additional of CREB siRNA, indicating the central role of CREB in CaMKIV-regulated processes.
The role of miRNAs in regulation of platelet activity and related diseases - a bioinformatic analysis
Published in Platelets, 2022
Zofia Wicik, Pamela Czajka, Ceren Eyileten, Alex Fitas, Marta Wolska, Daniel Jakubik, Dirk von Lewinski, Harald Sourij, Jolanta M. Siller-Matula, Marek Postula
CREB1 is a transcription factor inducing the transcription of genes in response to hormonal stimulation of the cyclic AMP (cAMP) pathway. It is known that cAMP can inhibit human platelet aggregation through the activation of a separate G protein-coupled pathway and platelet P2Y12 receptor [74]. There is still missing information about CAMP1ʹs role in platelets despite its association with platelet count in the Genome-wide association study (GWAS) catalog [75].
Mechanism of phthalate esters in the progression and development of breast cancer
Published in Drug and Chemical Toxicology, 2022
Mohd Mughees, Himanshu Chugh, Saima Wajid
Phthalate esters, like any other carcinogen, initiate a cascade of reactions inside a cell to induce and promote tumorigenesis. The pathway adopted by phthalate esters to induce cancer involves AhR-cAMP-PKA-CREB1 cascade. The aryl hydrocarbon receptor (AhR) is a ligand activated transcription factor associated with heat shock protein 90 (HSP 90). The AhR gets activated by halogentated aromatic hydrocarbon, polycyclic aromatic hydrocarbons and endogenous compounds in a dose dependent manner. The Tsung-Hua Hsieh et al. showed that BBP treated cells showed increased localization of AhR toward cell membrane (Hsieh et al.2012). This was associated with increased levels of cAMP and enhanced phosphorylation of CREB1 and a PKA inhibitor. Phthalates, hence triggers the AhR-cAMP-PKA-CREB1 cascade. This cascade further enhances the translation of gene HDAC6 (López-Carrillo et al. 2010). The HDAC6 is known to transcriptionally activates c-Myc via beta catenin-LEF/TCF4 in Er negative breast cancer cells. Transcriptional activation of C-Myc is associated with increased cell proliferation, cell migration and increased tumor growth (López-Carrillo et al.2010). The Ahr also cause transcriptional activation of CYP1b1. The CYP1b1 is a monooxygenase capable of metabolizing xenobiotics, it hydroxylates estradiol to 4-hydroxy estradiol which is then further oxidized to estrogen-3, 4 -semiquinone. 4-hydroxy estradiol is a potent carcinogen. This if accompanied with generation of reactive oxygen species and a DNA adduct would cause cancer or promote existing tumors. Besides this, CYP1b1 is known to target cell cycle apoptosis, cell adhesion by regulating cyclin E1, S-phase kinase associated protein 2, RAD52, p27 and cyclin e binding protein (Nicolopoulou-Stamati et al.2015). The Ahr via nongenomic pathways activates cox-2. up-regulated levels of Cox-2 with prostaglandin E2 associated with breast cancer (Nicolopoulou-Stamati et al.2015).