Journal articles: 'CerK'

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Schwalm, Stephanie, Martin Erhardt, Isolde Römer, Josef Pfeilschifter, Uwe Zangemeister-Wittke, and Andrea Huwiler. "Ceramide Kinase Is Upregulated in Metastatic Breast Cancer Cells and Contributes to Migration and Invasion by Activation of PI 3-Kinase and Akt." International Journal of Molecular Sciences 21, no. 4 (February 19, 2020): 1396. http://dx.doi.org/10.3390/ijms21041396.

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Ceramide kinase (CerK) is a lipid kinase that converts the proapoptotic ceramide to ceramide 1-phosphate, which has been proposed to have pro-malignant properties and regulate cell responses such as proliferation, migration, and inflammation. We used the parental human breast cancer cell line MDA-MB-231 and two single cell progenies derived from lung and bone metastasis upon injection of the parental cells into immuno-deficient mice. The lung and the bone metastatic cell lines showed a marked upregulation of CerK mRNA and activity when compared to the parental cell line. The metastatic cells also had increased migratory and invasive activity, which was dose-dependently reduced by the selective CerK inhibitor NVP-231. A similar reduction of migration was seen when CerK was stably downregulated with small hairpin RNA (shRNA). Conversely, overexpression of CerK in parental MDA-MB-231 cells enhanced migration, and this effect was also observed in the non-metastatic cell line MCF7 upon CerK overexpression. On the molecular level, CerK overexpression increased the activation of protein kinase Akt. The increased migration of CerK overexpressing cells was mitigated by the CerK inhibitor NVP-231, by inhibition of the phosphoinositide 3-kinase (PI3K)/Akt pathway and the Rho kinase, but not by inhibition of the classical extracellular signal-regulated kinase (ERK) pathway. Altogether, our data demonstrate for the first time that CerK promotes migration and invasion of metastatic breast cancer cells and that targeting of CerK has potential to counteract metastasis in breast cancer.

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Camacho, Laura, Amaia Zabala-Letona, Ana R. Cortazar, Ianire Astobiza, Asier Dominguez-Herrera, Amaia Ercilla, Jana Crespo, et al. "Identification of Androgen Receptor Metabolic Correlome Reveals the Repression of Ceramide Kinase by Androgens." Cancers 13, no. 17 (August 26, 2021): 4307. http://dx.doi.org/10.3390/cancers13174307.

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Prostate cancer (PCa) is one of the most prevalent cancers in men. Androgen receptor signaling plays a major role in this disease, and androgen deprivation therapy is a common therapeutic strategy in recurrent disease. Sphingolipid metabolism plays a central role in cell death, survival, and therapy resistance in cancer. Ceramide kinase (CERK) catalyzes the phosphorylation of ceramide to ceramide 1-phosphate, which regulates various cellular functions including cell growth and migration. Here we show that activated androgen receptor (AR) is a repressor of CERK expression. We undertook a bioinformatics strategy using PCa transcriptomics datasets to ascertain the metabolic alterations associated with AR activity. CERK was among the most prominent negatively correlated genes in our analysis. Interestingly, we demonstrated through various experimental approaches that activated AR reduces the mRNA expression of CERK: (i) expression of CERK is predominant in cell lines with low or negative AR activity; (ii) AR agonist and antagonist repress and induce CERK mRNA expression, respectively; (iii) orchiectomy in wildtype mice or mice with PCa (harboring prostate-specific Pten deletion) results in elevated Cerk mRNA levels in prostate tissue. Mechanistically, we found that AR represses CERK through interaction with its regulatory elements and that the transcriptional repressor EZH2 contributes to this process. In summary, we identify a repressive mode of AR that influences the expression of CERK in PCa.

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Ordoñez, Marta, Natalia Presa, Miguel Trueba, and Antonio Gomez-Muñoz. "Implication of Ceramide Kinase in Adipogenesis." Mediators of Inflammation 2017 (2017): 1–7. http://dx.doi.org/10.1155/2017/9374563.

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Ceramide kinase (CerK) plays a critical role in the regulation of cell growth and survival and has been implicated in proinflammatory responses. In this work, we demonstrate that CerK regulates adipocyte differentiation, a process associated with obesity, which causes chronic low-grade inflammation. CerK was upregulated during differentiation of 3T3-L1 preadipocytes into mature adipocytes. Noteworthy, knockdown of CerK using specific siRNA to silence the gene encoding this kinase resulted in substantial decrease of lipid droplet formation and potent depletion in the content of triacylglycerols in the adipocytes. Additionally, CerK knockdown caused blockade of leptin secretion, an adipokine that is crucial for regulation of energy balance in the organism and that is increased in the obese state. Moreover, CerK gene silencing decreased the expression of peroxisome proliferator-activated receptor gamma (PPARγ), which is considered the master regulator of adipogenesis. It can be concluded that CerK is a novel regulator of adipogenesis, an action that may have potential implications in the development of obesity, and that targeting this kinase may be beneficial for treatment of obesity-associated diseases.

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Rovina, Philipp, Markus Jaritz, Siegfried Höfinger, Christine Graf, Piroska Dévay, Andreas Billich, Thomas Baumruker, and Frédéric Bornancin. "A critical β6–β7 loop in the pleckstrin homology domain of ceramide kinase." Biochemical Journal 400, no. 2 (November 14, 2006): 255–65. http://dx.doi.org/10.1042/bj20060316.

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CerK (ceramide kinase) produces ceramide 1-phosphate, a sphingophospholipid with recognized signalling properties. It localizes to the Golgi complex and fractionates essentially between detergent-soluble and -insoluble fractions; however, the determinants are unknown. Here, we made a detailed mutagenesis study of the N-terminal PH domain (pleckstrin homology domain) of CerK, based on modelling, and identified key positively charged amino acid residues within an unusual motif in the loop interconnecting β-strands 6 and 7. These residues are critical for CerK membrane association and polyphosphoinositide binding and activity. Their mutagenesis results in increased thermolability, sensitivity to proteolysis, reduced apparent molecular mass as well as propensity of the recombinant mutant protein to aggregate, indicating that this loop impacts the overall conformation of the CerK protein. This is in contrast with most PH domains whose function strongly relies on charges located in the β1–β2 loop.

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Hinkovska-Galcheva, Vania T., Andrea J. Clark, Andrei L. Kindzelskii, Susan M. VanWay, JiBiao Huang, Thomas P. Shanley, James A. Shayman, Howard R. Petty, and Laurence A. Boxer. "Ceramide Kinase Promotes Store Dependent Ca2+ Signals and Enhances Phagolysosomal Fusion in COS-1 Cells." Blood 108, no. 11 (November 16, 2006): 1629. http://dx.doi.org/10.1182/blood.v108.11.1629.1629.

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Abstract We showed that ceramide-1-phosphate (C1P) is formed by ceramide kinase (CERK). In this study the mechanism by which C1P enhanced phagocytosis and phagolysosomal formation in COS-1 cells expressing hCERK was evaluated. We hypothesized that CERK has a unique role in inducing Ca2+ signaling during Fc-mediated phagocytosis via its generation of C1P. Furthermore, we also hypothesize that CERK mediated changes in Ca2+ levels were not direct but required the participation of a store operated channels (SOC). In some systems, evidence suggests that SOC might be related to transient receptor potential channel (TRP) homologues. This hypothesis was tested using cell lines with different levels of expression of CERK and by using series of pharmacological inhibitors. To monitor subcellular localization of hCERK, red fluorescent protein (RFP)-tagged hCERK was created and confocal microscopy was performed. To study dynamic changes in Ca2+ during phagocytosis, imaging microscopy was used. Phagolysosome formation was evaluated by labeling the cells with lysotracker red DND-99 at 37oC and followed by imaging. When challenged with EIgG, hCERK transfected cells increased phagocytosis and simultaneously increased C1P. During subcellular fractionation of hCERK transfected cells, CERK translocates during activation from the cytosol to a lipid raft fraction. We also observed that TRP-1 accumulated at the site of CERK translocation in lipid rafts. Microfluorimetry of indo-1 revealed that Ca2+ oscillations in COS-1 cells, stably transfected with Fcγ RIIA/hCERK, were much higher compared to Fcγ RIIA transfected cells. The enhanced Ca2+ signals were accompanied by enhanced phagolysosome formation. hCERK transfected cells had a mean rate of fusion of 90%, compare to 76% ( catalytic inactive mutant of CERK-G198DhCERK), 65% (Fcγ RIIA), and 70% (Vector) transfected cells. The indo-1 intensity spikes demonstrated significantly higher Ca2+ intensities for phagosomes associated with the hCERK transfectants. The SOC inhibitor SKF96365 blocked enhanced Ca2+ signaling in the hCERK transfected cells. Similarly SOC inhibitors reduced the phagocytic index and phagolysosomal fusion in hCERK transfected cells. Our data showed that there is a co-localization of EIgG and CERK as well as caveolin-1 and CERK on the surface of the phagocytic cells. Site directed mutagenesis demonstrated that the kinase activity of hCERK was required for higher Ca2+ signals. Pharmacological inhibitors revealed that this Ca2+ signal operates through SOC. Our results show that introduction of the hCERK gene in cells alters the functional behavior of intracellular signals and supports the role of C1P in promoting membrane fusion by modulating Ca2+ signaling through activation of SOC

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Rajput, Kajal, Mohammad Nafees Ansari, Somesh K. Jha, Trishna Pani, Nihal Medatwal, Somdeb Chattopadhyay, Avinash Bajaj, and Ujjaini Dasgupta. "Ceramide Kinase (CERK) Emerges as a Common Therapeutic Target for Triple Positive and Triple Negative Breast Cancer Cells." Cancers 14, no. 18 (September 16, 2022): 4496. http://dx.doi.org/10.3390/cancers14184496.

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Sphingolipids are key signaling biomolecules that play a distinct role in cell proliferation, migration, invasion, drug resistance, metastasis, and apoptosis. Triple-negative (ER−PR−HER2−) and triple-positive (ER+PR+HER2+) breast cancer (called TNBC and TPBC, respectively) subtypes reveal distinct phenotypic characteristics and responses to therapy. Here, we present the sphingolipid profiles of BT-474 and MDA-MB-231 breast cancer cell lines representing the TPBC and TNBC subtypes. We correlated the level of different classes of sphingolipids and the expression of their corresponding metabolizing enzymes with the cell proliferation and cell migration properties of BT-474 and MDA-MB-231 cells. Our results showed that each cell type exhibits a unique sphingolipid profile, and common enzymes such as ceramide kinase (CERK, responsible for the synthesis of ceramide-1-phosphates) are deregulated in these cell types. We showed that siRNA/small molecule-mediated inhibition of CERK can alleviate cell proliferation in BT-474 and MDA-MB-231 cells, and cell migration in MDA-MB-231 cells. We further demonstrated that nanoparticle-mediated delivery of CERK siRNA and hydrogel-mediated sustained delivery of CERK inhibitor to the tumor site can inhibit tumor progression in BT-474 and MDA-MB-231 tumor models. In summary, distinct sphingolipid profiles of TPBC and TNBC representing cell lines provide potential therapeutic targets such as CERK, and nanoparticle/hydrogel mediated pharmacological manipulations of such targets can be explored for future cancer therapeutics.

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Pierucci, Federica, Alessia Frati, Chiara Battistini, Fabio Penna, Paola Costelli, and Elisabetta Meacci. "Control of Skeletal Muscle Atrophy Associated to Cancer or Corticosteroids by Ceramide Kinase." Cancers 13, no. 13 (June 30, 2021): 3285. http://dx.doi.org/10.3390/cancers13133285.

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Apart from cytokines and chemokines, sphingolipid mediators, particularly sphingosine-1-phosphate (S1P) and ceramide 1-phosphate (C1P), contribute to cancer and inflammation. Cancer, as well as other inflammatory conditions, are associated with skeletal muscle (SkM) atrophy, which is characterized by the unbalance between protein synthesis and degradation. Although the signaling pathways involved in SkM mass wasting are multiple, the regulatory role of simple sphingolipids is limited. Here, we report the impairment of ceramide kinase (CerK), the enzyme responsible for the phosphorylation of ceramide to C1P, associated with the accomplishment of atrophic phenotype in various experimental models of SkM atrophy: in vivo animal model bearing the C26 adenocarcinoma or Lewis lung carcinoma tumors, in human and murine SkM cells treated with the conditioned medium obtained from cancer cells or with the glucocorticoid dexamethasone. Notably, we demonstrate in all the three experimental approaches a drastic decrease of CerK expression. Gene silencing of CerK promotes the up-regulation of atrogin-1/MAFbx expression, which was also observed after cell treatment with C8-ceramide, a biologically active ceramide analogue. Conversely, C1P treatment significantly reduced the corticosteroid’s effects. Altogether, these findings provide evidence that CerK, acting as a molecular modulator, may be a new possible target for SkM mass regulation associated with cancer or corticosteroids.

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Camacho, Laura, Alberto Ouro, Ana Gomez-Larrauri, Arkaitz Carracedo, and Antonio Gomez-Muñoz. "Implication of Ceramide Kinase/C1P in Cancer Development and Progression." Cancers 14, no. 1 (January 4, 2022): 227. http://dx.doi.org/10.3390/cancers14010227.

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Cancer cells rewire their metabolic programs to favor biological processes that promote cell survival, proliferation, and dissemination. Among this relevant reprogramming, sphingolipid metabolism provides metabolites that can favor or oppose these hallmarks of cancer. The sphingolipid ceramide 1-phosphate (C1P) and the enzyme responsible for its biosynthesis, ceramide kinase (CERK), are well established regulators of cell growth and survival in normal, as well as malignant cells through stress-regulated signaling pathways. This metabolite also promotes cell survival, which has been associated with the feedback regulation of other antitumoral sphingolipids or second messengers. C1P also regulates cancer cell invasion and migration of different types of cancer, including lung, breast, pancreas, prostate, or leukemia cells. More recently, CERK and C1P have been implicated in the control of inflammatory responses. The present review provides an updated view on the important role of CERK/C1P in the regulation of cancer cell growth, survival, and dissemination.

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Pal, Purab, Alec Millner, Svetlana E. Semina, Rosemary J. Huggins, Logan Running, Diana S. Aga, Debra A. Tonetti, et al. "Endocrine Therapy-Resistant Breast Cancer Cells Are More Sensitive to Ceramide Kinase Inhibition and Elevated Ceramide Levels Than Therapy-Sensitive Breast Cancer Cells." Cancers 14, no. 10 (May 12, 2022): 2380. http://dx.doi.org/10.3390/cancers14102380.

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ET resistance is a critical problem for estrogen receptor-positive (ER+) breast cancer. In this study, we have investigated how alterations in sphingolipids promote cell survival in ET-resistant breast cancer. We have performed LC-MS-based targeted sphingolipidomics of tamoxifen-sensitive and -resistant MCF-7 breast cancer cell lines. Follow-up studies included treatments of cell lines and patient-derived xenograft organoids (PDxO) with small molecule inhibitors; cytometric analyses to measure cell death, proliferation, and apoptosis; siRNA-mediated knockdown; RT-qPCR and Western blot for gene and protein expression; targeted lipid analysis; and lipid addback experiments. We found that tamoxifen-resistant cells have lower levels of ceramides and hexosylceramides compared to their tamoxifen-sensitive counterpart. Upon perturbing the sphingolipid pathway with small molecule inhibitors of key enzymes, we identified that CERK is essential for tamoxifen-resistant breast cancer cell survival, as well as a fulvestrant-resistant PDxO. CERK inhibition induces ceramide-mediated cell death in tamoxifen-resistant cells. Ceramide-1-phosphate (C1P) partially reverses CERK inhibition-induced cell death in tamoxifen-resistant cells, likely through lowering endogenous ceramide levels. Our findings suggest that ET-resistant breast cancer cells maintain lower ceramide levels as an essential pro-survival mechanism. Consequently, ET-resistant breast cancer models have a unique dependence on CERK as its activity can inhibit de novo ceramide production.

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Van Overloop, Helena, Gerd Van der Hoeven, and Paul P. Van Veldhoven. "A Nonradioactive Fluorimetric SPE-Based Ceramide Kinase Assay Using NBD-C6-Ceramide." Journal of Lipids 2012 (2012): 1–9. http://dx.doi.org/10.1155/2012/404513.

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Ceramide kinase (CERK) has been implicated in important cellular processes such as inflammation and apoptosis. Its activity is usually measured using radiolabeled ceramide or [γ-32P]-ATP, followed by extraction, thin-layer chromatography, and detection of the formed labeled ceramide-1-phosphate. To eliminate the use of radioactivity, we developed similarly but independently from the approach by Don and Rosen (2008), a fluorescence-based ceramide kinase assay, using N-[7-(4-nitrobenz-2-oxa-1,3-diazole)]-6-aminohexanoyl-sphingenine (NBD-C6-ceramide) as substrate. ItsKmvalue (4 μM) was comparable to that of N-hexanoyl-sphingenine (C6-ceramide). The produced fluorescent NBD-C6-ceramide-1-phosphate was captured by means of solid-phase extraction on an aminopropyl phase, resulting in a fast and sensitive CERK measurement. By performing this assay in a 96-well format, it is also suitable for high-throughput screening (HTS) to search for CERK modulators. A limited screen revealed that some protein kinase inhibitors (e.g., U-0126;IC504 μM) and ceramide analogues (e.g., fenretinide, AMG-9810;IC501.1 μM) affect CERKin vitro.

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Pal, Purab, Alec Millner, Ekin Atilla-Gokcumen, and Jonna Frasor. "Abstract P4-02-06: Exploiting ceramide homeostasis to target endocrine therapy-resistant breast cancer." Cancer Research 82, no. 4_Supplement (February 15, 2022): P4–02–06—P4–02–06. http://dx.doi.org/10.1158/1538-7445.sabcs21-p4-02-06.

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Abstract Estrogen receptor (ER)-positive breast cancer accounts for the majority of breast cancer-related deaths. Current treatment includes endocrine therapy (ET), which most women respond to at first. However, up to 40% of women will eventually experience a relapse. Recurrent tumors tend to retain ER expression but no longer respond to ET. There have been multiple genomic and proteomic profiling studies between ET-sensitive and ET-resistant breast cancer cells, but lipidomic studies have been lacking. We have performed targeted and non-targeted lipidomic profiling of ET-sensitive and two models of ET-resistant MCF-7 breast cancer cells and found differences in their sphingolipid profiles, suggesting our overarching hypothesis that ceramide homeostasis is altered in ET-resistance. The current study is designed to understand the functional role of ceramides and their metabolites in ET-resistant breast cancer, with an overall goal to improve the current treatment regimens and quality of life in breast cancer patients. Detection of ceramides and other sphingolipid levels were analyzed by reverse-phase chromatography and LC-QToF-MS. C1P levels were detected by LC-QqQ-MS. Hoechst-PI staining was performed to measure cell death and Annexin-PI staining to detect apoptosis. All cytometric data analyses were performed using a Celigo cytometer. RT-qPCR was performed to analyze mRNA expression. Fold changes were calculated using the ΔΔCt method with multiple housekeeping controls. While numerous changes were observed in lipid species, the most pronounced changes were seen in the sphingolipidome. More specifically, ET-resistant breast cancer cells had lower levels of ceramides and di-hydroceramides. Along with a depletion of ceramides, we have also observed an increase in ceramide-1-phosphate (C1P) levels in the ET-resistant cells. C1P, which is produced by phosphorylation of ceramides by ceramide kinase (CERK), is known to promote cell survival and proliferation. This observation suggests that ET-resistant cells may rely on a higher degree of ceramide turnover to C1P compared to their ET-sensitive counterpart. To test this hypothesis, CERK was inhibited with a small molecule inhibitor (NVP-231), which resulted in increased apoptosis in ET-resistant cells but not in ET-sensitive cells, suggesting ET-resistant cells are more sensitive to CERK inhibition. Although NVP-231 treatment increased ceramide levels in both ET-sensitive and ET-resistant cells, only ET-resistant cells were dependent on ceramide turnover to C1P. To further understand the molecular underpinnings of the differential sensitivity to CERK inhibition, we have investigated the expression of several BCL2 family members, as evidence from the literature suggests that sphingolipids play a critical role in apoptosis by interacting with several BCL2 family members by mechanisms that are not thoroughly understood. We have observed a high positive correlation between BCL2 expression and NVP-231 sensitivity, as well as an inverse correlation between MCL-1 and NVP-231 sensitivity. This suggests that loss of BCL2 in the ET-resistant cells may be a factor for increased sensitivity to CERK inhibition and elevated MCL-1 fails to compensate for that loss. Together, our findings suggest that ET-resistant breast cancer cells have a unique ceramide homeostasis dependence, i.e., rely on a higher degree of ceramide turnover to C1P. Additionally, BCL2 family proteins may play a critical role in determining the sensitivity to CERK inhibition. The dependence of ET-resistant breast cancer cells on C1P production for survival can therefore offer a unique opportunity to increase the therapeutic efficacy and improve patient outcome for women with ET-resistant breast cancer. Citation Format: Purab Pal, Alec Millner, Ekin Atilla-Gokcumen, Jonna Frasor. Exploiting ceramide homeostasis to target endocrine therapy-resistant breast cancer [abstract]. In: Proceedings of the 2021 San Antonio Breast Cancer Symposium; 2021 Dec 7-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2022;82(4 Suppl):Abstract nr P4-02-06.

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Ku, Chee Wai, Joan Yang, Hong Ying Tan, Jerry Kok Yen Chan, and Yie Hou Lee. "Decreased Innate Migration of Pro-Inflammatory M1 Macrophages through the Mesothelial Membrane Is Affected by Ceramide Kinase and Ceramide 1-P." International Journal of Molecular Sciences 23, no. 24 (December 15, 2022): 15977. http://dx.doi.org/10.3390/ijms232415977.

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The retrograde flow of endometrial tissues deposited into the peritoneal cavity occurs in women during menstruation. Classically (M1) or alternatively (M2) activated macrophages partake in the removal of regurgitated menstrual tissue. The failure of macrophage egress from the peritoneal cavity through the mesothelium leads to chronic inflammation in endometriosis. To study the migration differences of macrophage phenotypes across mesothelial cells, an in vitro model of macrophage egress across a peritoneal mesothelial cell monolayer membrane was developed. M1 macrophages were more sessile, emigrating 2.9-fold less than M2 macrophages. The M1 macrophages displayed a pro-inflammatory cytokine signature, including IL-1α, IL-1β, TNF-α, TNF-β, and IL-12p70. Mass spectrometry sphingolipidomics revealed decreased levels of ceramide-1-phosphate (C1P), an inducer of migration in M1 macrophages, which correlated with its poor migration behavior. C1P is generated by ceramide kinase (CERK) from ceramide, and blocking C1P synthesis via the action of NVP231, a specific CERK chemical inhibitor, prohibited the emigration of M1 and M2 macrophages up to 6.7-fold. Incubation with exogenously added C1P rescued this effect. These results suggest that M1 macrophages are less mobile and have higher retention in the peritoneum due to lower C1P levels, which contributes to an altered peritoneal environment in endometriosis by generating a predominant pro-inflammatory cytokine environment.

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Hinkovska-Galcheva, Vania, Susan M. Van Way, Timothy Cornell, Lei Sun, Iana Gueorguieva, and Nikolay Zlatarov. "Synergistic effect of TNF-α and ceramide on the production of IL-8 in A549 cells and A549 cells transfected with human ceramide kinase (CERK). (90.11)." Journal of Immunology 178, no. 1_Supplement (April 1, 2007): S158—S159. http://dx.doi.org/10.4049/jimmunol.178.supp.90.11.

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Abstract Many inducers of the stress response result in ceramide (Cer) accumulation as a result of activation of either sphingolyelinases (SMases) or the de novo pathway. Recently, there is strong evidence for a role of sphingolipids in inflammatory responses such as leukocyte recruitment. The attraction of leukocytes to tissues is essential for inflammation and the host response to infection. Following stimulation by TNF-?, the production of IL-8 increased over time in a concentration dependent manner. Simultaneously, Cer levels increased gradually from 7.56 % during 15 minute stimulation to 35% for 16 hour stimulation. Using Fumonisin B1, an inhibitor of de novo synthesis of Cer, which inhibits Cer synthesis by 25%, we observed 17% decrease of IL-8 expression. When the inhibitor for neutral (SMase) GW4869 was used on A549 cells, there was a significant reduction of Cer as well as IL-8. Subsequently, two serine-threonine phosphatases (PPas), protein phosphatase-1 (PP1) and protein phosphatase-2A (PP2A) have been shown to be Cer responsive in vitro and in vivo. These results suggest that TNF-? stimulates the production of IL-8 by a mechanism that involves the sphingomyelin-Cer system. Cer may be important in increasing the production of IL-8 in A 549 cells. Since Cer can be phosphorylated by CERK to C1P, we predict that CERK expression may affect the balance between these sphingolipids and influence the Cer dependent PPas.

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Yu, Wei-Li, and Yun Sun. "CERK inhibition might be a good potential therapeutic target for diseases." British Journal of Pharmacology 172, no. 8 (March 16, 2015): 2165. http://dx.doi.org/10.1111/bph.13017.

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Gomez-Larrauri, Ana, Natalia Presa, Asier Dominguez-Herrera, Alberto Ouro, Miguel Trueba, and Antonio Gomez-Muñoz. "Role of bioactive sphingolipids in physiology and pathology." Essays in Biochemistry 64, no. 3 (June 24, 2020): 579–89. http://dx.doi.org/10.1042/ebc20190091.

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Abstract Sphingolipids are a class of complex lipids containing a backbone of sphingoid bases, namely the organic aliphatic amino alcohol sphingosine (Sph), that are essential constituents of eukaryotic cells. They were first described as major components of cell membrane architecture, but it is now well established that some sphingolipids are bioactive and can regulate key biological functions. These include cell growth and survival, cell differentiation, angiogenesis, autophagy, cell migration, or organogenesis. Furthermore, some bioactive sphingolipids are implicated in pathological processes including inflammation-associated illnesses such as atherosclerosis, rheumatoid arthritis, inflammatory bowel disease (namely Crohn’s disease and ulcerative colitis), type II diabetes, obesity, and cancer. A major sphingolipid metabolite is ceramide, which is the core of sphingolipid metabolism and can act as second messenger, especially when it is produced at the plasma membrane of cells. Ceramides promote cell cycle arrest and apoptosis. However, ceramide 1-phosphate (C1P), the product of ceramide kinase (CerK), and Sph 1-phosphate (S1P), which is generated by the action of Sph kinases (SphK), stimulate cell proliferation and inhibit apoptosis. Recently, C1P has been implicated in the spontaneous migration of cells from some types of cancer, and can enhance cell migration/invasion of malignant cells through interaction with a Gi protein-coupled receptor. In addition, CerK and SphK are implicated in inflammatory responses, some of which are associated with cancer progression and metastasis. Hence, targeting these sphingolipid kinases to inhibit C1P or S1P production, or blockade of their receptors might contribute to the development of novel therapeutic strategies to reduce metabolic alterations and disease.

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Huang, Renliang, Zheng Li, Cui Mao, Hui Zhang, Zhongfeng Sun, Hao Li, Congcong Huang, et al. "Natural variation at Os CERK 1 regulates arbuscular mycorrhizal symbiosis in rice." New Phytologist 225, no. 4 (October 3, 2019): 1762–76. http://dx.doi.org/10.1111/nph.16158.

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Huang, Jin-lu, Yan Huo, Li-li Wan, Quan-jun Yang, Jie Li, and Cheng Guo. "CERK might contribute to inflammatory pain; Comments on Yu WL, Sun. Y (2015). CERK inhibition might be a good potential therapeutic target for diseases. Br J Pharmacol 172: 2165." British Journal of Pharmacology 173, no. 7 (March 18, 2016): 1248–49. http://dx.doi.org/10.1111/bph.13443.

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Dimopoulos, Nicolas, Ricco Tindjau, Darren C. J. Wong, Till Matzat, Tegan Haslam, Changzheng Song, Gregory A. Gambetta, Ljerka Kunst, and Simone D. Castellarin. "Drought stress modulates cuticular wax composition of the grape berry." Journal of Experimental Botany 71, no. 10 (January 27, 2020): 3126–41. http://dx.doi.org/10.1093/jxb/eraa046.

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Abstract Drought events are a major challenge for many horticultural crops, including grapes, which are often cultivated in dry and warm climates. It is not understood how the cuticle contributes to the grape berry response to water deficit (WD); furthermore, the cuticular waxes and the related biosynthetic pathways are poorly characterized in this fruit. In this study, we identified candidate wax-related genes from the grapevine genome by phylogenetic and transcriptomic analyses. Developmental and stress response expression patterns of these candidates were characterized across pre-existing RNA sequencing data sets and confirmed a high responsiveness of the pathway to environmental stresses. We then characterized the developmental and WD-induced changes in berry cuticular wax composition, and quantified differences in berry transpiration. Cuticular aliphatic wax content was modulated during development and an increase was observed under WD, with wax esters being strongly up-regulated. These compositional changes were related to up-regulated candidate genes of the aliphatic wax biosynthetic pathway, including CER10, CER2, CER3, CER1, CER4, and WSD1. The effect of WD on berry transpiration was not significant. This study indicates that changes in cuticular wax amount and composition are part of the metabolic response of the grape berry to WD, but these changes do not reduce berry transpiration.

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Yamada, Kenta, Koji Yamaguchi, Tomomi Shirakawa, Hirofumi Nakagami, Akira Mine, Kazuya Ishikawa, Masayuki Fujiwara, et al. "The Arabidopsis CERK 1‐associated kinase PBL 27 connects chitin perception to MAPK activation." EMBO Journal 35, no. 22 (September 27, 2016): 2468–83. http://dx.doi.org/10.15252/embj.201694248.

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Espinoza, Catherine, Yan Liang, and Gary Stacey. "Chitin receptor CERK 1 links salt stress and chitin‐triggered innate immunity in Arabidopsis." Plant Journal 89, no. 5 (February 8, 2017): 984–95. http://dx.doi.org/10.1111/tpj.13437.

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QIN, Fu-niu, Jing CONG, Shi-jun HU, and Xiao-huan LIANG. "Expression of Ceramide Kinase (Cerk) and Related Regulation in Early Pregnant Uterus of Mice." Journal of Reproduction and Contraception 22, no. 2 (June 2011): 113–25. http://dx.doi.org/10.1016/s1001-7844(11)60013-8.

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ALRASHED, FATEMA, and RASHEED AHMAD. "200-LB: Ceramide Kinase CERK Regulates Inflammatory Responses in Monocytes/Macrophages Induced by TNF-a." Diabetes 69, Supplement 1 (June 2020): 200—LB. http://dx.doi.org/10.2337/db20-200-lb.

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Rawat, Prigya, Prigya Rawat, Vinay Singh, and Vinay Singh. "Circular Bio-Economy Voyage." International Journal of Social Ecology and Sustainable Development 13, no. 7 (December 2022): 1–21. http://dx.doi.org/10.4018/ijsesd.290392.

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The circular bio-economy journey is determined exceedingly from the industrial ecological lens, with brief intake from the management field studies. The present research embarks to contemplate the circular bio-economy applying managerial approach by splitting the complicated abstraction into a more straightforward structure using VOS Viewer software. Nine determining elements backed by organizational vantage point are extracted - industrial symbiosis, sustainable transitions, multilevel perspective, bio-economic regions, governance, innovations, challenges, sustainability and regional value chains. All nine elements retrieved from the literature are ranked based on expert opinion. Eventually, variable CER6 (challenges) ranked first in the order, followed by CER1 (sustainable transitions); the least relevant variable ranked by the experts is CER9 (industrial symbiosis). For better validation, the TISM technique is used. These pressing issues demand immediate attention from practitioners, entrepreneurs, policy-makers, academicians, and management scholars.

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Hu, Chun-Hong, Peng-Qi Wang, Peng-Peng Zhang, Xiu-Min Nie, Bin-Bin Li, Li Tai, Wen-Ting Liu, Wen-Qiang Li, and Kun-Ming Chen. "NADPH Oxidases: The Vital Performers and Center Hubs during Plant Growth and Signaling." Cells 9, no. 2 (February 13, 2020): 437. http://dx.doi.org/10.3390/cells9020437.

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NADPH oxidases (NOXs), mostly known as respiratory burst oxidase homologs (RBOHs), are the key producers of reactive oxygen species (ROS) in plants. A lot of literature has addressed ROS signaling in plant development regulation and stress responses as well as on the enzyme’s structure, evolution, function, regulation and associated mechanisms, manifesting the role of NOXs/RBOHs as the vital performers and center hubs during plant growth and signaling. This review focuses on recent advances of NOXs/RBOHs on cell growth, hormone interaction, calcium signaling, abiotic stress responses, and immunity. Several primary particles, including Ca2+, CDPKs, BIK1, ROPs/RACs, CERK, FER, ANX, SnRK and SIK1-mediated regulatory mechanisms, are fully summarized to illustrate the signaling behavior of NOXs/RBOHs and their sophisticated and dexterous crosstalks. Diverse expression and activation regulation models endow NOXs/RBOHs powerful and versatile functions in plants to maintain innate immune homeostasis and development integrity. NOXs/RBOHs and their related regulatory items are the ideal targets for crop improvement in both yield and quality during agricultural practices.

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Mansfield, Pamela J., Vania Hinkovska-Galcheva, Michael Borofsky, James A. Shayman, and Laurence A. Boxer. "Phagocytic Signaling Molecules in Lipid Rafts of COS-1 Cells Transfected with FcγRIIA." Blood 104, no. 11 (November 16, 2004): 2384. http://dx.doi.org/10.1182/blood.v104.11.2384.2384.

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Abstract FcγRIIA-mediated phagocytosis involves a number of signaling proteins and lipids, which increasingly are viewed as localizing subcellularly in plasma membrane microdomains providing a framework for their interaction. COS-1 cells stably transfected with FcγRIIA were used as a model to demonstrate co-localization of several enzymes shown to be important in polymorphonuclear leukocyte (PMN) phagocytic signaling. Previously we developed a model wherein FcγRIIA engagement in PMNs resulted in activation of phospholipase D (PLD), producing phosphatidic acid, which is hydrolyzed to diglyceride, an activator of PKC. PKCδ and Raf-1 then activate the MAP kinase pathway and subsequently myosin to allow pseudopod formation. In COS-1 cells as in PMNs, PLD in the membrane fraction was activated during phagocytosis. COS-1 PLD was found almost exclusively in lipid rafts identified by the presence of caveolin, while two of its cofactors, RhoA and ARF1, were enriched in rafts. PKCδ and Raf-1 translocated to the plasma membrane, and were enriched in lipid rafts, reaching highest levels 5 to 10 min after phagocytosis was initiated. Rottlerin, a specific inhibitor of PKCδ, completely inhibited phagocytosis, suggesting that PKCδ regulates phagocytosis in COS-1 cells; however, translocation of PKCδ to rafts was not inhibited by rottlerin. Chelation of intracellular calcium with BAPTA-AM inhibited phagocytosis by only 25%, suggesting that PKCα or PKCβ, which both require calcium, were not important regulators of phagocytosis. A specific inhibitor of MEK (which is activated by Raf and activates MAP kinase), PD098059, inhibited phagocytosis by about 35%, suggesting that the MAP kinase pathway is involved in, but not the key factor required for, COS-1 cell phagocytosis. Extracellular signal-regulated kinase-2 (ERK2), a MAP kinase, was present in the raft fraction. In PMNs, phagocytosis and activation of MAP kinase are inhibited by exogenous ceramide, and endogenous ceramide levels increase during phagocytosis, indicating that FcγRIIA engagement initiates ceramide generation. Applying this model, we transfected COS-1 cells with FcγRIIA that had been mutated in the ITAM region (Y282F and Y298F), rendering them unable to ingest particles. When the mutant receptors were engaged, ceramide was generated and MAP kinase was activated normally, thus these processes did not require actual ingestion of particles. Previously we showed that ceramide 1-phosphate (C1P), the product of ceramide kinase (CERK), promotes membrane fusion in PMNs. Here we found that C1P increased in COS-1 cells during phagocytosis. CERK was found to be enriched in lipid rafts, translocating during phagocytosis. These results indicate that signaling proteins for phagocytosis are either constitutively present in, or are recruited to, lipid rafts where they are readily available to activate one another.

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Mitsutake, Susumu, and Yasuyuki Igarashi. "Sdudies of SMS2 or CerK deficiency mice and their relations to diet-induced obesity and mast cell activation." Chemistry and Physics of Lipids 163 (August 2010): S4. http://dx.doi.org/10.1016/j.chemphyslip.2010.05.014.

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Qi, Meng, Rui Wu, Zhihua Song, Biying Dong, Ting Chen, Mengying Wang, Hongyan Cao, et al. "Sorbitol Reduces Sensitivity to Alternaria by Promoting Ceramide Kinases (CERK) Expression through Transcription Factor Pswrky25 in Populus (Populus simonii Carr.)." Genes 13, no. 3 (February 24, 2022): 405. http://dx.doi.org/10.3390/genes13030405.

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Sugar, acting as a signal, can regulate the production of some chemical substance during plant defense responses. However, the molecular basis and regulatory mechanisms of sugar in poplar and other forest trees are still unclear. Sorbitol is a sugar-signaling molecule associated with plant defense. In this study, the pathogen-infested status of poplar was alleviated after exogenous feeding of 50 mM sorbitol. We sequenced and analyzed the transcriptome of poplar leaves before and after inoculation. The results showed that the genes PR1, WRKY, ceramide kinases (CERK) and so on responded to sorbitol feeding and pathogen infestation. We screened for genes related to disease resistance such as PsWRKY25 and PsCERK1 and found that significant disease spots occurred on day six of strep throat infestation. Under sorbitol feeding conditions, the appearance of spots was delayed after the pathogen inoculation. Due to the overexpression of PsWRKY25, the overexpression of PsCERK1 triggered the defense response in poplar. This was also confirmed by PsWRKY25 overexpression experiments. These findings present new insights into the influence of sorbitol on Populus simonii Carr. disease resistance. These results emphasize the value of molecular phenotypes in predicting physiological changes.

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Kukreti, Himani, and Kottaiswamy Amuthavalli. "MicroRNA‐34a causes ceramide accumulation and effects insulin signaling pathway by targeting ceramide kinase ( CERK ) in aging skeletal muscle." Journal of Cellular Biochemistry 121, no. 5-6 (June 2020): 3070–89. http://dx.doi.org/10.1002/jcb.29312.

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Pope, Joan. "50-YEAR HISTORY OF THE UNITED STATES (USA) ARMY ENGINEERS COASTAL ENGINEERING RESEARCH BOARD (CERB)." Coastal Engineering Proceedings, no. 36 (December 30, 2018): 70. http://dx.doi.org/10.9753/icce.v36.risk.70.

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The U. S. Army Coastal Engineering Research Board (CERB), established on 7 November 1963 by Public Law No. 172, of the 88th USA Congress, has had a major impact on the field and profession of coastal engineering for over 50 years. The CERB replaced the Beach Erosion Board (BEB) (created in 1930) and provided oversight to the Coastal Engineering Research Center (CERC), now the Coastal and Hydraulics Laboratory. The greatest names in USA coastal engineering and science have served on the CERB and helped to define the course of USA coastal research and practice.

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Khoza, Thembisile, Ian Dubery, and Lizelle Piater. "Identification of Candidate Ergosterol-Responsive Proteins Associated with the Plasma Membrane of Arabidopsis thaliana." International Journal of Molecular Sciences 20, no. 6 (March 14, 2019): 1302. http://dx.doi.org/10.3390/ijms20061302.

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The impact of fungal diseases on crop production negatively reflects on sustainable food production and overall economic health. Ergosterol is the major sterol component in fungal membranes and regarded as a general elicitor or microbe-associated molecular pattern (MAMP) molecule. Although plant responses to ergosterol have been reported, the perception mechanism is still unknown. Here, Arabidopsis thaliana protein fractions were used to identify those differentially regulated following ergosterol treatment; additionally, they were subjected to affinity-based chromatography enrichment strategies to capture and categorize ergosterol-interacting candidate proteins using liquid chromatography coupled with tandem mass spectrometry (LC-MS/MS). Mature plants were treated with 250 nM ergosterol over a 24 h period, and plasma membrane-associated fractions were isolated. In addition, ergosterol was immobilized on two different affinity-based systems to capture interacting proteins/complexes. This resulted in the identification of defense-related proteins such as chitin elicitor receptor kinase (CERK), non-race specific disease resistance/harpin-induced (NDR1/HIN1)-like protein, Ras-related proteins, aquaporins, remorin protein, leucine-rich repeat (LRR)- receptor like kinases (RLKs), G-type lectin S-receptor-like serine/threonine-protein kinase (GsSRK), and glycosylphosphatidylinositol (GPI)-anchored protein. Furthermore, the results elucidated unknown signaling responses to this MAMP, including endocytosis, and other similarities to those previously reported for bacterial flagellin, lipopolysaccharides, and fungal chitin.

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Hait, Nitai C., and Aparna Maiti. "The Role of Sphingosine-1-Phosphate and Ceramide-1-Phosphate in Inflammation and Cancer." Mediators of Inflammation 2017 (2017): 1–17. http://dx.doi.org/10.1155/2017/4806541.

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Inflammation is part of our body’s response to tissue injury and pathogens. It helps to recruit various immune cells to the site of inflammation and activates the production of mediators to mobilize systemic protective processes. However, chronic inflammation can increase the risk of diseases like cancer. Apart from cytokines and chemokines, lipid mediators, particularly sphingosine-1-phosphate (S1P) and ceramide-1-phosphate (C1P), contribute to inflammation and cancer. S1P is an important player in inflammation-associated colon cancer progression. On the other hand, C1P has been recognized to be involved in cancer cell growth, migration, survival, and inflammation. However, whether C1P is involved in inflammation-associated cancer is not yet established. In contrast, few studies have also suggested that S1P and C1P are involved in anti-inflammatory pathways regulated in certain cell types. Ceramide is the substrate for ceramide kinase (CERK) to yield C1P, and sphingosine is phosphorylated to S1P by sphingosine kinases (SphKs). Biological functions of sphingolipid metabolites have been studied extensively. Ceramide is associated with cell growth inhibition and enhancement of apoptosis while S1P and C1P are associated with enhancement of cell growth and survival. Altogether, S1P and C1P are important regulators of ceramide level and cell fate. This review focuses on S1P and C1P involvement in inflammation and cancer with emphasis on recent progress in the field.

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Kızılkonca, Ezgi, and F. Bedia Erim. "Development of Anti-Aging and Anticorrosive Nanoceria Dispersed Alkyd Coating for Decorative and Industrial Purposes." Coatings 9, no. 10 (September 25, 2019): 610. http://dx.doi.org/10.3390/coatings9100610.

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This study focuses on nano cerium oxide particles as alternative additives in solvent-based alkyd coatings in order to improve anticorrosive and anti-aging properties. The paint samples were formulated with cerium oxide micro and nanoparticles, and the coating quality characteristics were compared with coating formulated with commercial anticorrosive and UV-aging agents. Formulations were prepared with 3 wt % commercial anticorrosive agent as reference material (RP), 3 wt % cerium oxide microparticles (CER1), 3 wt % and 1% cerium oxide nanoparticles (CER2 and CER3), respectively. The basket milling technique with zirconium balls was used for the preparations of coatings and characterizations were performed by Fourier transform infrared spectroscopy (FTIR), thermogravimetric analysis (TGA), and contact angle measurements. Improvement in the anticorrosive properties was proven with electrochemical impedance spectroscopy (EIS) and accelerated salt spray tests based on ISO 4628 Evaluation of Degradation of Coatings. Furthermore, physical and mechanical tests were run according to standard test methods for coatings and reported. Results showed that cerium oxide particles provide anticorrosive, UV defender, and self-cleaning effects, besides excellent physical resistance to alkyd coatings. The impact of cerium oxide nanoparticles was found to be stronger than those of the microparticles.

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Wang, Jian, Li Zhang, Kunling Teng, Shutao Sun, Zhizeng Sun, and Jin Zhong. "Cerecidins, Novel Lantibiotics from Bacillus cereus with Potent Antimicrobial Activity." Applied and Environmental Microbiology 80, no. 8 (February 14, 2014): 2633–43. http://dx.doi.org/10.1128/aem.03751-13.

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ABSTRACTLantibiotics are ribosomally synthesized and posttranslationally modified antimicrobial peptides that are widely produced by Gram-positive bacteria, including many species of theBacillusgroup. In the present study, one novel gene cluster coding lantibiotic cerecidins was unveiled inBacillus cereusstrain As 1.1846 through genomic mining and PCR screening. The designatedcerlocus is different from that of conventional class II lantibiotics in that it included seven tandem precursorcerAgenes, one modification gene (cerM), two processing genes (cerTandcerP), one orphan regulator gene (cerR), and two immunity genes (cerFandcerE). In addition, one unprecedented quorum sensing component,comQXPA, was inserted betweencerMandcerR. The expression of cerecidins was not detected in this strain ofB. cereus, which might be due to repressed transcription ofcerM. We constitutively coexpressedcerAgenes andcerMinEscherichia coli, and purified precerecidins were proteolytically processed with the endoproteinase GluC and a truncated version of putative serine protease CerP. Thus, two natural variants of cerecidins A1 and A7 were obtained which contained two terminal nonoverlapping thioether rings rarely found in lantibiotics. Both cerecidins A1 and A7 were active against a broad spectrum of Gram-positive bacteria. Cerecidin A7, especially its mutant Dhb13A, showed remarkable efficacy against multidrug-resistantStaphylococcus aureus(MDRSA), vancomycin-resistantEnterococcus faecalis(VRE), and evenStreptomyces.

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McNevin, John P., Wendy Woodward, Abdelali Hannoufa, Kenneth A. Feldmann, and Bertrand Lemieux. "Isolation and characterization of eceriferum (cer) mutants induced by T-DNA insertions in Arabidopsis thaliana." Genome 36, no. 3 (June 1, 1993): 610–18. http://dx.doi.org/10.1139/g93-082.

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Thirteen Arabidopsis thaliana mutants with deviating epicuticular wax layers (i.e., cer mutants) were isolated by screening 13 000 transformed lines produced by the seed transformation method. After crossing the 13 mutants to some of the previously known cer mutant lines, 12 of our mutants mapped to 6 of the 21 known complementation groups (cer1 through cer4 as well as cer6 and cer10), while the other mutant corresponded to a previously unknown locus, cer21. Mutant phenotypes of 6 of the 13 mutant lines were caused by T-DNA insertions within cer genes. We also analyzed the chemical composition of the epicuticular wax layers of the cer mutants isolated in this study relative to that of Arabidopsis wild-type plants. Our results suggest that the five genes we tagged regulate different steps in wax biosynthesis, i.e., the decarbonylation of fatty aldehydes to alkanes, the elongation of hexacosanoic acid to octacosanoic acid, the reduction of fatty aldehydes to primary alcohols and the production of free aldehydes, while an insertion in the fifth gene causes an alteration in the chain length distribution of the different classes of wax compounds.Key words: epicuticular wax, glossy mutants, gas chromotography – mass spectroscopy.

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García-Oliva, Carlos, José Antonio Piqueras Rodríguez, and Juan Carlos Marzo Campos. "Uso problemático de Internet, el móvil y los videojuegos en una muestra de adolescentes alicantinos." Health and Addictions/Salud y Drogas 17, no. 2 (July 23, 2017): 189–200. http://dx.doi.org/10.21134/haaj.v17i2.331.

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El uso habitual de las Tecnologías de la Información y la Comunicación (TICs) está especialmente consolidado en población adolescente y juvenil, generando en algunos casos consecuencias negativas para el individuo. El objetivo del presente estudio es explorar los usos generales y los usos problemáticos que los adolescentes alicantinos hacen de las TICs más populares: Internet, teléfono móvil y videojuegos. La muestra estuvo formada por 319 adolescentes alicantinos entre 12 y 18 años. Se administraron los Cuestionarios de Experiencias Relacionadas con Internet, el Móvil y Videojuegos (CERI, CERM y CERV), que valoran los usos problemáticos de estas tecnologías, así como medidas ad-hoc para evaluar la frecuencia de uso y los usos más comunes. Los resultados muestran que en torno al 10% de la muestra presenta puntuaciones elevadas en uso problemático en cada una de las tecnologías, y un 2.2% de la muestra presenta problemas de uso en dos medios simultáneamente. Por último, se exponen las diferencias halladas según edad y sexo en cada uno de los usos. Estos datos suponen una aproximación al fenómeno del uso problemático de las TICs en adolescentes; se requiere estudios específicos para establecer los factores de riesgo de los usos problemáticos de internet, móvil y videojuegos

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Muñoz-Navarro, Roger, Antonio Cano Vindel, Florian Schmitz, Rosario Cabello, and Pablo Fernández-Berrocal. "Emotional Disorders During the COVID-19 Outbreak in Spain: The Role of Sociodemographic Risk Factors and Cognitive Emotion Regulation Strategies." Health Education & Behavior 48, no. 4 (May 19, 2021): 412–23. http://dx.doi.org/10.1177/10901981211014101.

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Background Cognitive emotion regulation strategies (CERS) play a transdiagnostic role in emotional disorders, but the role of these strategies in coping with emotions during the coronavirus disease 2019 (COVID-19) pandemic remains poorly understood. Aims To assess the presence of emotional disorders in Spain and the association to sociodemographic characteristics and CERS during the COVID-19 outbreak. Method Cross-sectional survey administered through an online platform. Sociodemographic variables and CERS (CERQ-Short) were collected and possible diagnoses of generalized anxiety disorder (GAD, GAD-7), major depression disorder (MDD; Patient Health Questionnaire–9 [PHQ-9]), panic attacks (PA; PHQ-PD), and panic disorders (PD; PHQ-PD) were assessed. Sociodemographic risk factors and CERS association to the possible diagnosis of emotional disorders were reported with hierarchical multivariate logistic regression analyses. Results A total of 1,753 respondents completed the questionnaire in Spain. Of these, most (76.8%) were female, with a mean ( SD) age of 40.4 years (12.9). A high proportion of participants met diagnostic criteria for emotional disorders: 15.3% for GAD, 12.2% for MDD, 17.2% for PD, and 25.7% had experienced a PA. The contribution of sociodemographic variables to diagnoses of emotional disorders was modest, explaining from 3.1% to 5.7% of the variance; however, when CERS were added, the combination of sociodemographic and CERS explained from 15% to 29% of the variance. Rumination and catastrophizing were the most transdiagnostic maladaptive strategies and positive refocusing was another adaptive strategy. Discussion Although results from convenience samples should be handled with caution, the high prevalence of emotional disorders in this study suggests that the demand of mental health interventions will probably increase in Spain. Also, CERS play a clear role in the presence of these disorders. Conclusion Intervention programs should focus on training CERS in populations at high risk, focusing on the reduction of maladaptive CERS and the reinforce of other more adaptive CERS.

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Humphreys, Aimee, Hanna Russell, and Helen L. Fillmore. "DIPG-50. Bioinformatic evaluation of genes involved in sphingomyelin biosynthesis in Diffuse Midline Glioma H3K27 altered/DIPG: dysregulation of sphingosine 1-phosphate (SP1)." Neuro-Oncology 24, Supplement_1 (June 1, 2022): i30. http://dx.doi.org/10.1093/neuonc/noac079.107.

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Abstract Sphingosine 1-phosphate (S1P), a bioactive signalling lipid, interacts with a network of metabolic enzymes, receptors, transporters, and epigenetic partners. This network is well described in many cancers; however, little is known about its potential impact in DIPG. Expression of HDAC1 (binding target of S1P) and genes associated with the sphingomyelin (SM) pathway were examined in datasets identified in the National Centre for Biotechnology Information, Gene Expression Omnibus, and analysed using the R2: Genomics Analysis and Visualization Platform (http://r2.amc.nl). The Paugh-DIPG dataset (27 DIPG samples) and normal samples (20 years and younger - Berchtold dataset) were compared. To avoid issues related to batch effects, expression values for each gene of interest and controls were exported into separate files to determine differentially expressed genes. Internal genes include housekeeping; ACTB, GAPDH, B2M, TBP; downregulated in DIPG; GPR6, NGB, and upregulated in DIPG; MMP16, PDGFRA, TP53, CSPG4. Genes of interest; SPHK1, SPHK2, SGPL1, ACER1, ACER3, KDSR, SMPD1-4, CPTP, GLTP, DEGS1, CERK, CERS1-6, ASAH1, SGPP1, SGPP2 and HDAC1. To test for significance, each dataset was standardised using ACTB housekeeping gene. Values including Log-transformed fold change were analysed using the non-parametric, Mann-Whitney test. 7 of the 16 genes were dysregulated relative to expression in normal brain (p<0.0002). SPHK2 and SMPD3 were downregulated, and HDAC1, SGPL1, DEGS1, CERS4, and ASAH1 were upregulated in DIPG compared to normal. To identify genes more likely associated with DIPG (vs development), we evaluated gene expression in Brainspan dataset (brspv10rs). Validation of SPHK2 and SGPL1 protein expression (responsible for the synthesis and cleavage of SP1) is underway. Current work is focused on the intracellular processing and function (isoform specific inhibitors) of S1P in DIPG cells. Given its reported role in several cancer hallmarks, a better understanding of the sphingomyelin biosynthesis pathway in DMG/DIPG is merited and may lead to novel therapeutic targets.

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Muy-Rangel, Dolores, Jorge Siller-Cepeda, Juan Díaz-Pérez, and Benigno Valdéz-Torres. "EFECTO DE LAS CONDICIONES DE ALMACENAMIENTO Y EL ENCERADO EN EL ESTATUS HÍDRICO Y LA CALIDAD POSCOSECHA DE PEPINO DE MESA." Revista Fitotecnia Mexicana 27, no. 2 (August 2, 2022): 157. http://dx.doi.org/10.35196/rfm.2004.2.157.

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Las condiciones de almacenamiento y la aplicación de cera que influyen en el estatus hídrico y la calidad poscosecha de frutos de pepino (Cucumis sativus L.) cv. Conquistador, se investigaron para generar modelos empíricos que permitan predecir calidad y vida de anaquel. Los frutos se almacenaron bajo seis diferentes condiciones de déficit de presión de vapor (DPV desde 0.19 hasta 1.26 kPa). Se midieron pérdidas de peso diaria y acumulativa, firmeza, potenciales hídrico (Ψw), osmótico (Ψs) y de presión (Ψp), así como sólidos solubles totales y contenido relativo de agua (CRA). Los primeros síntomas de pérdida de calidad (marchitamiento) se notaron cuando los frutos alcanzaron 6 % de pérdida de peso, independiente de las condiciones de DPV o de la aplicación de cera. El uso de cera redujo la pérdida de peso en las distintas condiciones de almacenamiento, en comparación con los frutos sin encerar. La pérdida de peso diaria de frutos con y sin cera en función de las condiciones de almacenamiento (DPV) permitió generar modelos para predecir la pérdida de peso. Los frutos encerados en condiciones de baja humedad relativa (DPV=1.26 kPa), alcanzaron 6 % de pérdida de peso a los 6 d, mientras que en alta humedad relativa (DPV = 0.2 kPa) los frutos (con o sin cera) no presentaron estas pérdidas. Al inicio, los potenciales hídrico, osmótico y de presión en el fruto mostraron valores de -0.4 MPa, -0.6 MPa y +0.2 MPa, respectivamente, y durante el almacenamiento los frutos redujeron sus valores de Ψw y Ψs, particularmente en baja humedad relativa. El contenido relativo de agua (CRA) disminuyó por encima de 10 % durante el almacenamiento. Valores inferiores a 88 % de CRA indicaron plasmólisis celular, causada por la disminución en el valor del Ψp de cero o menor.

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Prokopovich, D. A., M. I. Reinhard, I. M. Cornelius, and A. B. Rosenfeld. "Geant4 simulation of the CERN-EU high-energy reference field (CERF) facility." Radiation Protection Dosimetry 141, no. 2 (May 28, 2010): 106–13. http://dx.doi.org/10.1093/rpd/ncq152.

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Silari, Marco, and Fabio Pozzi. "The CERN-EU high-energy Reference Field (CERF) facility: applications and latest developments." EPJ Web of Conferences 153 (2017): 03001. http://dx.doi.org/10.1051/epjconf/201715303001.

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Brall, T., M. Dommert, W. Rühm, S. Trinkl, M. Wielunski, and V. Mares. "Monte Carlo simulation of the CERN-EU High Energy Reference Field (CERF) facility." Radiation Measurements 133 (April 2020): 106294. http://dx.doi.org/10.1016/j.radmeas.2020.106294.

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Caresana, M., M. Ferrarini, A. Parravicini, and A. Sashala Naik. "Dose measurements with CR-39 detectors at the CERF reference facility at CERN." Radiation Measurements 71 (December 2014): 502–4. http://dx.doi.org/10.1016/j.radmeas.2014.04.010.

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Vicente-Escudero, José Luis, Pedro Saura-Garre, Concepción López-Soler, Antonia Martínez, and Mavi Alcántara. "Adicción al móvil e internet en adolescentes y su relación con problemas psicopatológicos y variables protectoras." Escritos de Psicología - Psychological Writings 12, no. 2 (December 31, 2019): 103–12. http://dx.doi.org/10.24310/espsiescpsi.v12i2.10065.

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Se analizó la relación entre psicopatología y abuso del móvil e internet en adolescentes, además, se analizaron si ciertas variables protectoras de psicopatología protegen también del abuso del móvil e internet y se calcularon los puntos de corte dos cuestionarios que miden el abuso de estas tecnologías. Se empleó una muestra de 269 adolescentes entre 12 y 18 años (124 chicos y 145 chicas) y se usaron los cuestionarios YSR para medir psicopatología, CERI abuso de internet y CERM abuso del móvil. Los resultados mostraron que el abuso de las nuevas tecnologías se relaciona con sintomatología externalizante y de déficit de atención. Se halló que el número de clubs a los que pertenecen, relación con los padres, autonomía y rendimiento escolar en ciencias, son variables protectoras frente al abuso del móvil e internet. Además, a los 15 años aumenta significativamente el uso de estas tecnologías y la psicopatología asociada.

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Jiménez Torres, Miguel. "Globalization, Development without... zero?" Gestión y Estrategia 09 (January 1, 1996): 49–63. http://dx.doi.org/10.24275/uam/azc/dcsh/gye/1996n09/jimenez.

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Caresana, M., M. Helmecke, J. Kubancak, G. P. Manessi, K. Ott, R. Scherpelz, and M. Silari. "Instrument intercomparison in the high-energy mixed field at the CERN-EU reference field (CERF) facility." Radiation Protection Dosimetry 161, no. 1-4 (November 28, 2013): 67–72. http://dx.doi.org/10.1093/rpd/nct312.

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SAHLINS, MARSHALL. "Cery Cery fuckabede." American Ethnologist 20, no. 4 (November 1993): 848–67. http://dx.doi.org/10.1525/ae.1993.20.4.02a00100.

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Nurani, Indah Asikin. "Pola Komunitas Gua Di Sampung, Ponorogo." Berkala Arkeologi 23, no. 2 (November 11, 2003): 1–14. http://dx.doi.org/10.30883/jba.v23i2.871.

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Masing-masing gua/ceruk menunjukkan bahwa pemanfaatan lahan gua antara Gua Lawa dengan Ceruk Layah, Ceruk Ngalen, dan Ceruk Sulur menunjukkan perbedaan yang mencolok. Tampaknya Gua Lawa pada komunitas ini dimanfaatkan sebagai gua induk, di mana seluruh aktivitas komunitas berlangsung. Sementara itu Ceruk Layah, Ceruk Ngalen, dan Ceruk Sulur dimanfaatkan untuk aktivitas pendukung. Hal tersebut didasarkan pada perbandingan hasil ekskavasi antara Gua Lawa dengan ceruk-ceruk sekitarnya. Temuan artefak, ekofak dan fitur pada Gua Lawa lebih bervariasi baik kualitas maupun kuantitasnya dibanding ceruk-ceruk sekitarnya yang temuannya cenderung homogen berupa artefak litik. Selain itu, berdasarkan temuan artefak pada Ceruk Layah menunjukkan adanya perkembangan pemanfaatan ceruk. Pada awalnya (lapisan bawah) Ceruk Layah dimanfaatkan sebagai perbengkelan alat batu, selanjutnya pada masa kemudian (lapisan atas) didorninasi temuan tembikar. Sementara temuan ekofak pada ceruk-ceruk sekitar Gua Lawa cenderung minim. Hal tersebut dapat disirnpulkan bahwa pola kornunitas gua di Sampung terdiri atas gua induk dengan kompleksitas budaya yang berlangsung dan gua/ceruk pendukung yang dimanfaatkan untuk aktivitas sekunder.

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48

Gryniov, B. V., M. P. Titov, and P. O. Stadnyk. "Ukraine - СERN: the Way to Cooperation." Nauka ta innovacii 15, no. 5 (October 10, 2019): 93–105. http://dx.doi.org/10.15407/scin15.05.093.

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Agosteo, S., R. Bedogni, M. Caresana, N. Charitonidis, M. Chiti, A. Esposito, M. Ferrarini, C. Severino, and M. Silari. "Characterization of extended range Bonner Sphere Spectrometers in the CERF high-energy broad neutron field at CERN." Nuclear Instruments and Methods in Physics Research Section A: Accelerators, Spectrometers, Detectors and Associated Equipment 694 (December 2012): 55–68. http://dx.doi.org/10.1016/j.nima.2012.06.055.

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Eisner, G., V. Negruk, A. Hannoufa, and B. Lemieux. "Analysis of Arabidopsis thaliana transgenic plants transformed with CER2 and CER3 genes in sense and antisense orientations." Theoretical and Applied Genetics 97, no. 5-6 (October 1998): 801–9. http://dx.doi.org/10.1007/s001220050959.

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Journal articles on the topic 'CerK'

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