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Journal articles on the topic 'PRODH'

Author: Grafiati

Published: 4 June 2021

Last updated: 9 February 2022

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1

Zheng, Haitao, Leyi Lin, Yosuke Okezaki, Ryushi Kawakami, Haruhiko Sakuraba, Toshihisa Ohshima, Keiichi Takagi, and Shin-ichiro Suye. "Electrochemical behavior of dye-linked L-proline dehydrogenase on glassy carbon electrodes modified by multi-walled carbon nanotubes." Beilstein Journal of Nanotechnology 1 (December 14, 2010): 135–41. http://dx.doi.org/10.3762/bjnano.1.16.

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A glassy carbon electrode (GC) was modified by multi-walled carbon nanotubes (MWCNTs). The modified electrode showed a pair of redox peaks that resulted from the oxygen-containing functional groups on the nanotube surface. A recombinant thermostable dye-linked L-proline dehydrogenase (L-proDH) from hyperthermophilic archaeon (Thermococcus profundus) was further immobilized by physical adsorption. The modified electrode (GC/MWCNTs/L-proDH) exhibited an electrocatalytic signal for L-proline compared to bare GC, GC/L-proDH and GC/MWCNTs electrodes, which suggested that the presence of MWCNTs efficiently enhances electron transfer between the active site of enzyme and electrode surface. The immobilized L-proDH showed a typical Michaelis–Menten catalytic response with lower apparent constant.

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2

Fabro, Georgina, Yanina Soledad Rizzi, and María Elena Alvarez. "Arabidopsis Proline Dehydrogenase Contributes to Flagellin-Mediated PAMP-Triggered Immunity by Affecting RBOHD." Molecular Plant-Microbe Interactions® 29, no. 8 (August 2016): 620–28. http://dx.doi.org/10.1094/mpmi-01-16-0003-r.

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Plants activate different defense systems to counteract the attack of microbial pathogens. Among them, the recognition of conserved microbial- or pathogen-associated molecular patterns (MAMPs or PAMPs) by pattern-recognition receptors stimulates MAMP- or PAMP-triggered immunity (PTI). In recent years, the elicitors, receptors, and signaling pathways leading to PTI have been extensively studied. However, the contribution of organelles to this program deserves further characterization. Here, we studied how processes altering the mitochondrial electron transport chain (mETC) influence PTI establishment. With particular emphasis, we evaluated the effect of proline dehydrogenase (ProDH), an enzyme that can load electrons into the mETC and regulate the cellular redox state. We found that mETC uncouplers (antimycin or rotenone) and manganese superoxide dismutase deficiency impair flg22-induced responses such as accumulation of reactive oxygen species (ROS) and bacterial growth limitation. ProDH mutants also reduce these defenses, decreasing callose deposition as well. Using ProDH inhibitors and ProDH inducers (exogenous Pro treatment), we showed that this enzyme modulates the generation of ROS by the plasma membrane respiratory burst NADPH oxidase homolog D. In this way, we contribute to the understanding of mitochondrial activities influencing early and late PTI responses and the coordination of the redox-associated mitochondrial enzyme ProDH with defense events initiated at the plasma membrane.

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3

Kazberuk, Adam, Ilona Zareba, Jerzy Palka, and Arkadiusz Surazynski. "A novel plausible mechanism of NSAIDs-induced apoptosis in cancer cells: the implication of proline oxidase and peroxisome proliferator-activated receptor." Pharmacological Reports 72, no. 5 (July 24, 2020): 1152–60. http://dx.doi.org/10.1007/s43440-020-00140-z.

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Abstract Although pharmaco-epidemiological studies provided evidence for the anticancer potential of non-steroidal anti-inflammatory drugs (NSAIDs), the mechanism of their anti-cancer activity is not known. Several lines of evidence suggest that proline dehydrogenase/proline oxidase (PRODH/POX) may represent a target for NSAIDs-dependent anti-cancer activity. PRODH/POX catalyzes conversion of proline into Δ1-pyrroline-5-carboxylate releasing ATP or reactive oxygen species for autophagy/apoptosis. Since NSAIDs are ligands of peroxisome proliferator-activated receptor (PPARs) and PPARs are implicated in PRODH/POX-dependent apoptosis we provided a hypothesis on the mechanism of NSAIDs-induced apoptosis in cancer cells.

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4

Bender, Hans-Ulrich, Shlomo Almashanu, Gary Steel, Chien-An Hu, Wei-Wen Lin, Alecia Willis, Ann Pulver, and David Valle. "Functional Consequences of PRODH Missense Mutations." American Journal of Human Genetics 76, no. 3 (March 2005): 409–20. http://dx.doi.org/10.1086/428142.

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5

Willis, Alecia, Hans Uli Bender, Gary Steel, and David Valle. "PRODH variants and risk for schizophrenia." Amino Acids 35, no. 4 (June 5, 2008): 673–79. http://dx.doi.org/10.1007/s00726-008-0111-0.

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6

Zareba, Ilona, Arkadiusz Surazynski, Marcin Chrusciel, Wojciech Miltyk, Milena Doroszko, Nafis Rahman, and Jerzy Palka. "Functional Consequences of Intracellular Proline Levels Manipulation Affecting PRODH/POX–Dependent Pro-Apoptotic Pathways in a Novel in Vitro Cell Culture Model." Cellular Physiology and Biochemistry 43, no. 2 (2017): 670–84. http://dx.doi.org/10.1159/000480653.

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Background/Aims: The effect of impaired intracellular proline availability for proline dehydrogenase/proline oxidase (PRODH/POX)-dependent apoptosis was studied. Methods: We generated a constitutively knocked-down PRODH/POX MCF-7 breast cancer cell line (MCF-7shPRODH/POX) as a model to analyze the functional consequences of impaired intracellular proline levels. We have used inhibitor of proline utilization in collagen biosynthesis, 2-metoxyestradiol (MOE), inhibitor of prolidase that generate proline, rapamycin (Rap) and glycyl-proline (GlyPro), substrate for prolidase. Collagen and DNA biosynthesis were evaluated by radiometric assays. Cell viability was determined using Nucleo-Counter NC-3000. The activity of prolidase was determined by colorimetric assay. Expression of proteins was assessed by Western blot and immunofluorescence bioimaging. Concentration of proline was analyzed by liquid chromatography with mass spectrometry. Results: PRODH/POX knockdown decreased DNA and collagen biosynthesis, whereas increased prolidase activity and intracellular proline level in MCF-7shPRODH/POX cells. All studied compounds decreased cell viability in MCF-7 and MCF-7shPRODH/POX cells. DNA biosynthesis was similarly inhibited by Rap and MOE in both cell lines, but GlyPro inhibited the process only in MCF-7shPRODH/POX and MOE+GlyPro only in MCF-7 cells. All the compounds inhibited collagen biosynthesis, increased prolidase activity and cytoplasmic proline level in MCF-7shPRODH/POX cells and contributed to the induction of pro-survival mode only in MCF-7shPRODH/POX cells. In contrast, all studied compounds upregulated expression of pro-apoptotic protein only in MCF-7 cells. Conclusion: PRODH/POX was confirmed as a driver of apoptosis and proved the eligibility of MCF-7shPRODH/POX cell line as a highly effective model to elucidate the different mechanisms underlying proline utilization or generation in PRODH/POX-dependent pro-apoptotic pathways.

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7

Wang, Jiacheng, Zhimin Xue, Chunting Hua, Jun Lin, Zhida Shen, Yinjing Song, Hangying Ying, Qingbo Lv, Meihui Wang, and Binquan Zhou. "Metabolomic Analysis of the Ameliorative Effect of Enhanced Proline Metabolism on Hypoxia-Induced Injury in Cardiomyocytes." Oxidative Medicine and Cellular Longevity 2020 (November 26, 2020): 1–15. http://dx.doi.org/10.1155/2020/8866946.

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Background. Coronary heart disease is currently the leading cause of death in humans. Its poor prognosis and high mortality are associated with myocardial ischemia, which leads to metabolic disorder-related cardiomyocyte apoptosis and reactive oxygen species (ROS) production. Previous cardiovascular metabolomics studies in humans and mice have shown that proline metabolism is severely altered after cardiomyocyte hypoxia. Proline dehydrogenase (PRODH) is located on the inner mitochondrial membrane and is an enzyme that catalyzes the first step of proline catabolism, which plays an important role in improving the cellular redox state. In vitro oxygen-glucose deprivation can mimic in vivo myocardial ischemic injury. This study is aimed at investigating whether enhancing proline metabolism by overexpressing PRODH can ameliorate hypoxia-induced injury in cardiomyocytes and to reveal the related altered metabolites and mechanistic pathway via untargeted metabolomics analysis. Methods and Results. First, through public database analysis and RT-qPCR and western blot analyses in a cardiomyocyte hypoxia model, we found that the expression of the proline-degrading enzyme PRODH was downregulated after myocardial infarction and hypoxia exposure. Second, LDH assays, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), DHE staining, flow cytometric apoptosis analysis with DCFH and Annexin V-FITC/PI, and western blot analysis were used to assess the injury level in cardiomyocytes. Enhanced proline metabolism induced by PRODH overexpression reduced the levels of reactive oxidative stress and apoptosis, whereas PRODH knockdown had the opposite effects. Third, untargeted metabolomics analysis revealed that the protective effect was associated with significant changes in metabolism linked to sphingolipid signaling pathways, unsaturated fatty acid biosynthesis, phosphocreatine, glutathione disulfide, aminoacyl-tRNA biosynthesis, and ABC transporters. Conclusions. Our study demonstrated a protective effect of enhanced proline metabolism in cardiomyocytes under hypoxia, providing a novel strategy for exploring new treatments for coronary heart disease.

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8

Raimondi, Ivan, Yari Ciribilli, Paola Monti, Alessandra Bisio, Loredano Pollegioni, Gilberto Fronza, Alberto Inga, and Paola Campomenosi. "P53 Family Members Modulate the Expression of PRODH, but Not PRODH2, via Intronic p53 Response Elements." PLoS ONE 8, no. 7 (July 8, 2013): e69152. http://dx.doi.org/10.1371/journal.pone.0069152.

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9

Sasada, Shinsuke, Yoshihiro Miyata, Yasuhiro Tsutani, Jun Hihara, and Morihito Okada. "Metabolomic analysis of dynamic response and drug resistance of gastric cancer cells to 5-fluorouracil." Journal of Clinical Oncology 31, no. 15_suppl (May 20, 2013): e22053-e22053. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.e22053.

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e22053 Background: Metabolomics has developed as an important new tool in cancer research. It is expected to lead to the discovery of biomarker candidates for cancer diagnosis and treatment. The current study aimed to perform a comprehensive metabolomic analysis of the intracellular dynamic responses of human gastric cancer cells to 5-fluorouracil (5-FU), referencing the mechanism of drug action and drug resistance. Methods: Small metabolites in gastric cancer cells and 5-FU–resistant cells were measured by liquid chromatography-mass spectrometry. Candidates for drug targets were selected according to the presence or absence of resistance, before and after 5-FU treatment. In addition, the gene expression of each candidate was assessed by reverse transcription-polymerase chain reaction. Results: The number of metabolites in cancer cells dramatically changed during short-term treatment with 5-FU. Particularly, proline was reduced to one-third of its original level and glutamate was increased by a factor of 3 after 3 h of treatment. The metabolic production of glutamate from proline proceeds by proline dehydrogenase (PRODH), producing superoxide. After 5-FU treatment, PRODH mRNA expression was upregulated 2-fold and production of superoxide was increased by a factor of 3. In 5-FU–resistant cells, proline and glutamate levels were less affected than in non-resistant cells, and PRODH mRNA expression and superoxide generation were not increased following treatment. Conclusions: The authors identified a candidate biomarker, PRODH, for drug effects using the metabolomic approach, a result that was confirmed by conventional methods. In the future, metabolomics will play an important role in the field of cancer research.

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10

Misiura, Magdalena, Ilona Ościłowska, Katarzyna Bielawska, Jerzy Pałka, and Wojciech Miltyk. "PRODH/POX-Dependent Celecoxib-Induced Apoptosis in MCF-7 Breast Cancer." Pharmaceuticals 14, no. 9 (August 29, 2021): 874. http://dx.doi.org/10.3390/ph14090874.

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Celecoxib (Cx), an inhibitor of cyclooxygenase 2, induces apoptosis of cancer cells. However, the mechanism of the chemopreventive effect remains not fully understood. We aimed to investigate the role of PRODH/POX that is involved in the regulation of apoptosis induced by celecoxib. MCF-7 breast cancer cell line and the corresponding MCF-7 cell line with silenced PRODH/POX (MCF-7shPRODH/POX) were used. The effects of Cx on cell viability, proliferation, and cell cycle were evaluated. The expressions of protein markers for apoptosis (Bax, caspase 9, and PARP) and autophagy (Atg5, Beclin 1, and LC3A/B) were investigated by Western immunoblotting. To analyze the proline metabolism, collagen biosynthesis, prolidase activity, proline concentration, and the expression of proline-related proteins were evaluated. The generation of ATP, ROS, and the ratio of NAD+/NADH and NADP+/NADPH were determined to test the effect of Cx on energetic metabolism in breast cancer cells. It has been found that Cx attenuated MCF-7 cell proliferation via arresting the cell cycle. Cx induced apoptosis in MCF-7 breast cancer cells, while in MCF-7shPRODH/POX, autophagy occurred more predominantly. In MCF-7 breast cancer cells, Cx affected proline metabolism through upregulation of proline biosynthesis, PRODH/POX and PYCRs expressions, PEPD activity, and downregulation of collagen biosynthesis. In MCF-7shPRODH/POX clones, these processes, as well as energetic metabolism, were remarkably suppressed. The data for the first time suggest that celecoxib induces apoptosis through upregulation of PRODH/POX in MCF-7 breast cancer cells.

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11

Dellero, Younes, Vanessa Clouet, Nathalie Marnet, Anthoni Pellizzaro, Sylvain Dechaumet, Marie-Françoise Niogret, and Alain Bouchereau. "Leaf status and environmental signals jointly regulate proline metabolism in winter oilseed rape." Journal of Experimental Botany 71, no. 6 (December 6, 2019): 2098–111. http://dx.doi.org/10.1093/jxb/erz538.

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Abstract Proline metabolism is an essential component of plant adaptation to multiple environmental stress conditions that is also known to participate in specific developmental phases, particularly in reproductive organs. Recent evidence suggested a possible role for proline catabolism in Brassica napus for nitrogen remobilization processes from source leaves at the vegetative stage. Here, we investigate transcript levels of Δ1-PYRROLINE-5-CARBOXYLATE SYNTHASE (P5CS) and PROLINE DEHYDROGENASE (ProDH) genes at the vegetative stage with respect to net proline biosynthesis and degradation fluxes in leaves having a different sink/source balance. We showed that the underexpression of three P5CS1 genes in source leaves was accompanied by a reduced commitment of de novo assimilated 15N towards proline biosynthesis and an overall depletion of free proline content. We found that the expression of ProDH genes was strongly induced by carbon starvation conditions (dark-induced senescence) compared with early senescing leaves. Our results suggested a role for proline catabolism in B. napus, but acting only at a late stage of senescence. In addition, we also identified some P5CS and ProDH genes that were differentially expressed during multiple processes (leaf status, dark to light transition, and stress response).

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12

Kyme, Christine. "Importance of COMT and PRODH in psychosis development." Nature Clinical Practice Neurology 2, no. 2 (February 2006): 63. http://dx.doi.org/10.1038/ncpneuro0078.

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13

Ota, Vanessa K., Fernanda T. Bellucco, Ary Gadelha, Marcos L. Santoro, Cristiano Noto, Denise M. Christofolini, Idaiane B. Assunção, et al. "PRODH Polymorphisms, Cortical Volumes and Thickness in Schizophrenia." PLoS ONE 9, no. 2 (February 3, 2014): e87686. http://dx.doi.org/10.1371/journal.pone.0087686.

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14

Williams, H. J., N. Williams, G. Spurlock, N. Norton, D. Ivanov, R. G. McCreadie, A. Preece, et al. "Association between PRODH and schizophrenia is not confirmed." Molecular Psychiatry 8, no. 7 (July 2003): 644–45. http://dx.doi.org/10.1038/sj.mp.4001276.

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15

Ohtsuki, T. "Failure to find association between PRODH deletion and schizophrenia." Schizophrenia Research 67, no. 1 (March 1, 2004): 111–13. http://dx.doi.org/10.1016/s0920-9964(03)00160-9.

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16

Tołoczko-Iwaniuk, Natalia, Dorota Dziemiańczyk-Pakieła, Katarzyna Celińska-Janowicz, Ilona Zaręba, Agnieszka Klupczyńska, Zenon J. Kokot, Beata Klaudia Nowaszewska, Joanna Reszeć, Jan Borys, and Wojciech Miltyk. "Proline-Dependent Induction of Apoptosis in Oral Squamous Cell Carcinoma (OSCC)—The Effect of Celecoxib." Cancers 12, no. 1 (January 6, 2020): 136. http://dx.doi.org/10.3390/cancers12010136.

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Background: Oral squamous cell carcinoma remains a significant worldwide public health challenge, associated with high morbidity and mortality. Treatment of this type of cancer lacks effective medication. Moreover, there are very few specific biomarkers that are useful in early diagnosis or treatment optimisation. Proline metabolism may prove to be of importance in the search for new treatment modalities. Methods: To evaluate the significance of proline metabolism in the development of oral cancer, proline concentration was assessed in oral cancer tissue and normal oral mucosa. The results were compared to the clinical stage and histological grade of the tumours. Moreover, the expression of proteins involved in proline metabolism via proline dehydrogenase/oxidase (PRODH/POX, PPARγ, HIF1-α) was determined. In the next stage of the study, conducted on cell lines of tongue cancer treated with celecoxib, the aforementioned factors involved in proline metabolism were evaluated. Cellular viability and cell proliferation, as well as apoptosis, were also assessed. Results: Our research results indicate that a high intracellular proline concentration and expression of factors involved in its metabolism correlate with the clinical stage and histological grade of oral cancer. Moreover, we are the first researchers to demonstrate that celecoxib can affect proline metabolism, causing an increase in pro-apoptotic factors (PRODH/POX, PPARγ), reducing the expression of HIF-1α and activating apoptosis. Conclusions: Proline metabolism, due to its involvement in the process of apoptosis, can be of great importance in anticancer therapy. It appears that celecoxib, which influences the PRODH/POX pathway, may be a promising therapeutic compound in oral cancer treatment.

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17

Jacquet, H. "PRODH mutations and hyperprolinemia in a subset of schizophrenic patients." Human Molecular Genetics 11, no. 19 (September 15, 2002): 2243–49. http://dx.doi.org/10.1093/hmg/11.19.2243.

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18

Li, Tao, Xiaohong Ma, Xun Hu, Yingcheng Wang, Chengying Yan, Huaqing Meng, Xiehe Liu, Timothea Toulopoulou, Robin M. Murray, and David A. Collier. "PRODH gene is associated with executive function in schizophrenic families." American Journal of Medical Genetics Part B: Neuropsychiatric Genetics 147B, no. 5 (July 5, 2008): 654–57. http://dx.doi.org/10.1002/ajmg.b.30648.

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19

Afenjar, Alexandra, Marie-Laure Moutard, Diane Doummar, Agnés Guët, Daniel Rabier, Anne-Isabelle Vermersch, Cyril Mignot, et al. "Early neurological phenotype in 4 children with biallelic PRODH mutations." Brain and Development 29, no. 9 (October 2007): 547–52. http://dx.doi.org/10.1016/j.braindev.2007.01.008.

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20

Sakuraba, Haruhiko, Yoshinori Takamatsu, Takenori Satomura, Ryushi Kawakami, and Toshihisa Ohshima. "Purification, Characterization, and Application of a Novel Dye-Linked l-Proline Dehydrogenase from a Hyperthermophilic Archaeon, Thermococcus profundus." Applied and Environmental Microbiology 67, no. 4 (April 1, 2001): 1470–75. http://dx.doi.org/10.1128/aem.67.4.1470-1475.2001.

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ABSTRACT The distribution of dye-linked l-amino acid dehydrogenases was investigated in several hyperthermophiles, and the activity of dye-linked l-proline dehydrogenase (dye-l-proDH, l-proline:acceptor oxidoreductase) was found in the crude extract of someThermococcales strains. The enzyme was purified to homogeneity from a hyperthermophilic archaeon, Thermococcus profundus DSM 9503, which exhibited the highest specific activity in the crude extract. The molecular mass of the enzyme was about 160 kDa, and the enzyme consisted of heterotetrameric subunits (α2 β2) with two different molecular masses of about 50 and 40 kDa. The N-terminal amino acid sequences of the α-subunit (50-kDa subunit) and the β-subunit (40-kDa subunit) were MRLTEHPILDFSERRGRKVTIHF and XRSEAKTVIIGGGIIGLSIAYNLAK, respectively. Dye-l-proDH was extraordinarily stable among the dye-linked dehydrogenases under various conditions: the enzyme retained its full activity upon incubation at 70°C for 10 min, and ca. 40% of the activity still remained after heating at 80°C for 120 min. The enzyme did not lose the activity upon incubation over a wide range of pHs from 4.0 to 10.0 at 50°C for 10 min. The enzyme exclusively catalyzed l-proline dehydrogenation using 2,6-dichloroindophenol (Cl2Ind) as an electron acceptor. The Michaelis constants for l-proline and Cl2Ind were determined to be 2.05 and 0.073 mM, respectively. The reaction product was identified as Δ1-pyrroline-5-carboxylate by thin-layer chromatography. The prosthetic group of the enzyme was identified as flavin adenine dinucleotide by high-pressure liquid chromatography. In addition, the simple and specific determination of l-proline at concentrations from 0.10 to 2.5 mM using the stable dye-l-proDH was achieved.

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21

Williams, H. J., N. Williams, G. Spurlock, N. Norton, S. Zammit, G. Kirov, M. J. Owen, and M. C. O'Donovan. "Detailed analysis of PRODH and PsPRODH reveals no association with schizophrenia." American Journal of Medical Genetics 120B, no. 1 (June 13, 2003): 42–46. http://dx.doi.org/10.1002/ajmg.b.20049.

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22

Guo, Xingzhi, Peng Tang, Caiping Yang, and Rui Li. "Proline dehydrogenase gene (PRODH) polymorphisms and schizophrenia susceptibility: a meta-analysis." Metabolic Brain Disease 33, no. 1 (October 18, 2017): 89–97. http://dx.doi.org/10.1007/s11011-017-0128-8.

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23

Li, Huiying, Lei Xing, Muchen Zhang, Jiaqi Wang, and Nan Zheng. "The Toxic Effects of Aflatoxin B1 and Aflatoxin M1 on Kidney through Regulating L-Proline and Downstream Apoptosis." BioMed Research International 2018 (August 12, 2018): 1–11. http://dx.doi.org/10.1155/2018/9074861.

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The toxic effects and potential mechanisms of aflatoxin B1 (AFB1), aflatoxin M1 (AFM1), and AFB1+AFM1 in the kidney were studied and compared in HEK 293 cells model and CD-1 mice model. The 35-day subacute toxicity mice model was constructed, biochemical indicators and kidney pathological staining were detected, kidney metabonomics detection was performed, and the metabolites were analyzed, and then the related toxicity mechanism was validated. Results showed that AFB1 (0.5 mg/kg), AFM1 (3.5 mg/kg), and AFB1 (0.5 mg/kg)+AFM1 (3.5 mg/kg) activated oxidative stress and caused renal damage. The relative concentration of the metabolite L-proline was found to be lower in aflatoxins treatment groups when compared with the control (P<0.05). Moreover, with the treatment of aflatoxins, proline dehydrogenase (PRODH) and proapoptotic factors (Bax, Caspase-3) were upregulated, while the inhibitor of apoptosis Bcl-2 was downregulated, at both the mRNA and the protein levels, comparing with the control (P<0.05). In addition, the combined effect of AFB1 and AFM1 was validated, for the toxicity of the combination was stronger than the other two groups. In conclusion, AFB1 and AFM1 caused kidney toxicity by activating oxidative stress through altering expression of PRODH and L-proline levels, which then induced downstream apoptosis.

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24

Moghadam, F. H., Z. H. A. Mehrabani, M. Amounajaf, S. Rahmanzadeh, F. Ghasemvand, A. S. Samghabadi, A. Nejadmoghaddam, and E. Omidinia. "Proline dehydrogenase (PRODH) gene polymorphisms and the risk of schizophrenia in Iranian populations." Ukrainian Biochemical Journal 92, no. 1 (February 7, 2020): 12–20. http://dx.doi.org/10.15407/ubj92.01.012.

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25

Monteoliva, Mariela, Yanina Rizzi, Nicolás Cecchini, Mohammad-Reza Hajirezaei, and María Alvarez. "Context of action of Proline Dehydrogenase (ProDH) in the Hypersensitive Response of Arabidopsis." BMC Plant Biology 14, no. 1 (2014): 21. http://dx.doi.org/10.1186/1471-2229-14-21.

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26

Jday, Asma, Kilani Ben Rejeb, Ines Slama, Kaouthar Saadallah, Marianne Bordenave, Séverine Planchais, Arnould Savouré, and Chedly Abdelly. "Effects of exogenous nitric oxide on growth, proline accumulation and antioxidant capacity in Cakile maritima seedlings subjected to water deficit stress." Functional Plant Biology 43, no. 10 (2016): 939. http://dx.doi.org/10.1071/fp15363.

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Nitric oxide (NO) – an endogenous signalling molecule in plants and animals – mediates responses to biotic and abiotic stresses. In the present study, we examined the role of exogenous application of NO in mediating stress responses in Cakile maritima Scop. seedlings under water deficit stress using sodium nitroprusside (SNP) as NO donor and as a pre-treatment before the application of stress. Water deficit stress was applied by withholding water for 14 days. Growth, leaf water content (LWC), osmotic potential (ψs), chlorophyll, malondialdehyde (MDA), electrolyte leakage (EL), proline and Δ1-pyrroline-5-carboxylate synthetase (P5CS) and proline dehydrogenase (ProDH) protein levels were determined. Enzyme activities involved in antioxidant activities (superoxide dismutase (SOD) and catalase (CAT)) were measured upon withholding water. The results showed that shoot biomass production was significantly decreased in plants subjected to water deficit stress alone. However, in water deficit stressed plants pre-treated with SNP, growth activity was improved and proline accumulation was significantly increased. Proline accumulation was concomitant with the stimulation of its biosynthesis as shown by the accumulation of P5CS proteins. Nevertheless, no significant change in ProDH protein levels was observed. Besides plants showed lower water deficit-induced lipid membrane degradation and oxidative stress after the pretreatment with 100 µM SNP. This behaviour was related to the increased activity of SOD and CAT. Thus, we concluded that NO increased C. maritima drought tolerance and mitigated damage associated with water deficit stress by the regulation of proline metabolism and the reduction of oxidative damage.

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27

Prata, Diana Pinto, Gerome Breen, Janet Munro, Maggie Sinclair, Sarah Osborne, Tao Li, Robert Kerwin, David St. Clair, and David A. Collier. "Bipolar 1 disorder is not associated with the RGS4, PRODH, COMT and GRK3 genes." Psychiatric Genetics 16, no. 6 (December 2006): 229–30. http://dx.doi.org/10.1097/01.ypg.0000242190.43773.ce.

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28

Jacquet, H. "The severe form of type I hyperprolinaemia results from homozygous inactivation of the PRODH gene." Journal of Medical Genetics 40, no. 1 (January 1, 2003): 7e—7. http://dx.doi.org/10.1136/jmg.40.1.e7.

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29

Suntsova, M., E. V. Gogvadze, S. Salozhin, N. Gaifullin, F. Eroshkin, S. E. Dmitriev, N. Martynova, et al. "Human-specific endogenous retroviral insert serves as an enhancer for the schizophrenia-linked gene PRODH." Proceedings of the National Academy of Sciences 110, no. 48 (November 11, 2013): 19472–77. http://dx.doi.org/10.1073/pnas.1318172110.

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30

Sehgal, Sheikh Arslan. "Pharmacoinformatics and molecular docking studies reveal potential novel Proline Dehydrogenase (PRODH) compounds for Schizophrenia inhibition." Medicinal Chemistry Research 26, no. 2 (November 19, 2016): 314–26. http://dx.doi.org/10.1007/s00044-016-1752-2.

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31

Roussos, Panos, Stella G. Giakoumaki, and Panos Bitsios. "A Risk PRODH Haplotype Affects Sensorimotor Gating, Memory, Schizotypy, and Anxiety in Healthy Male Subjects." Biological Psychiatry 65, no. 12 (June 2009): 1063–70. http://dx.doi.org/10.1016/j.biopsych.2009.01.003.

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Karimian, Seyedeh Sara, Mohammad Taghi Akbari, Seyed Saeed Sadr, and Gholamreza Javadi. "Association of Candidate Single Nucleotide Polymorphisms Related to Candidate Genes in Patients With Schizophrenia." Basic and Clinical Neuroscience Journal 11, no. 5 (September 1, 2020): 595–608. http://dx.doi.org/10.32598/bcn.9.10.470.

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Introduction: Schizophrenia is a chronic heterogenic neurodevelopment disorder. Many genes interfere in the development of SCZ. All four genes, NrCAM, PRODH, ANK3, and ANKK1, which were evaluated in this study, were previously reported to be associated with Schizophrenia. The NrCAM contributes to creating cognitive deficiencies through the CAM’s signaling pathway. PRODH plays a vital role in creating SCZ negative symptoms through the signaling pathway of glutamatergic and NMDA receptors. ANK3 affects ion channel and molecular adhesion in Ranvier and initial segments of axons, leading to mental retardation, sleep disorder, and SCZ. ANKK1 encodes a protein kinase and was reported to be associated with alcohol addiction, Attention Deficit Hyperactivity Disorder (ADHD), and SCZ. Methods: The subjects were selected from Schizophrenic patients referring to the Psychiatric Ward of Imam-Hussein Hospital and Schizophrenic Patients Support Institution (AHEBBA). 95 (30 Schizoaffective patients, 57 Paranoid patients, and 8 disorganized) patients were recruited as the subjects in the present case-control association study. 120 healthy subjects were recruited from the Tehran Medical Genetics Laboratory staff and a group of students from the Islamic Azad University of Science and Research in Tehran. The genotypes were determined with molecular genotyping techniques of PCR-RFLP, ARMS-PCR, and Cycle sequencing. Results were analyzed by the Chi-Square test using SPSS V. 24 and R, SNP STATE Package to investigate significant differences between cases and controls. Results: The incidence of schizophrenia was 68% and 32% among men and women, respectively. The evaluation of the allelic association between schizophrenia and all the candidate SNPs showed a significant association between NrCAM's SNP rs10235968 and SCZ (P=0.001). Haplotype T, T, C in rs10235968, rs6967368, rs3763463, respectively, within the NrCAM gene, showed significant association with schizophrenia disorder (P=0.0001). Conclusion: No association was found between other candidate SNPs and SCZ among the subjects.

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Fang, Huan, Guangshi Du, Qiuju Wu, Rong Liu, Ceshi Chen, and Jing Feng. "HDAC inhibitors induce proline dehydrogenase (POX) transcription and anti-apoptotic autophagy in triple negative breast cancer." Acta Biochimica et Biophysica Sinica 51, no. 10 (September 6, 2019): 1064–70. http://dx.doi.org/10.1093/abbs/gmz097.

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Abstract Triple-negative breast cancer (TNBC) is the most aggressive subtype of breast cancer with poor clinical outcomes and without effective targeted therapies. Numerous studies have suggested that HDAC inhibitors (TSA/SAHA) may be effective in TNBCs. Proline oxidase, also known as proline dehydrogenase (POX/PRODH), is a key enzyme in the proline metabolism pathway and plays a vital role in tumorigenesis. In this study, we found that HDAC inhibitors (TSA/SAHA) significantly increased POX expression and autophagy through activating AMPK. Depletion of POX decreased autophagy and increased apoptosis induced by HDAC inhibitors in TNBC cells. These results suggest that POX contributes to cell survival under chemotherapeutic stresses and might serve as a potential target for treatment of TNBC.

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Zarchi, Omer, Miri Carmel, Chen Avni, Josef Attias, Amos Frisch, Elena Michaelovsky, Miriam Patya, et al. "Schizophrenia-like neurophysiological abnormalities in 22q11.2 deletion syndrome and their association to COMT and PRODH genotypes." Journal of Psychiatric Research 47, no. 11 (November 2013): 1623–29. http://dx.doi.org/10.1016/j.jpsychires.2013.07.004.

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Qin, Xianzheng, Jiang Chen, and Tian Zhou. "22q11.2 deletion syndrome and schizophrenia." Acta Biochimica et Biophysica Sinica 52, no. 11 (October 30, 2020): 1181–90. http://dx.doi.org/10.1093/abbs/gmaa113.

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Abstract 22q11.2 deletion is a common microdeletion that causes an array of developmental defects including 22q11.2 deletion syndrome (22q11DS) or DiGeorge syndrome and velocardiofacial syndrome. About 30% of patients with 22q11.2 deletion develop schizophrenia. Mice with deletion of the ortholog region in mouse chromosome 16qA13 exhibit schizophrenia-like abnormal behaviors. It is suggested that the genes deleted in 22q11DS are involved in the pathogenesis of schizophrenia. Among these genes, COMT, ZDHHC8, DGCR8, and PRODH have been identified as schizophrenia susceptibility genes. And DGCR2 is also found to be associated with schizophrenia. In this review, we focused on these five genes and reviewed their functions in the brain and the potential pathophysiological mechanisms in schizophrenia, which will give us a deeper understanding of the pathology of schizophrenia.

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Carmel, Miri, Omer Zarchi, Elena Michaelovsky, Amos Frisch, Miriam Patya, Tamar Green, Doron Gothelf, and Abraham Weizman. "Association of COMT and PRODH gene variants with intelligence quotient (IQ) and executive functions in 22q11.2DS subjects." Journal of Psychiatric Research 56 (September 2014): 28–35. http://dx.doi.org/10.1016/j.jpsychires.2014.04.019.

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Radoeva, Petya D., Ioana L. Coman, Cynthia A. Salazar, Karen L. Gentile, Anne Marie Higgins, Frank A. Middleton, Kevin M. Antshel, et al. "Association between autism spectrum disorder in individuals with velocardiofacial (22q11.2 deletion) syndrome and PRODH and COMT genotypes." Psychiatric Genetics 24, no. 6 (December 2014): 269–72. http://dx.doi.org/10.1097/ypg.0000000000000062.

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Di Rosa, Gabriella, Giuseppina Pustorino, Maria Spano, Dominique Campion, Marilena Calabrò, Mohammed Aguennouz, Daniela Caccamo, et al. "Type I hyperprolinemia and proline dehydrogenase (PRODH) mutations in four Italian children with epilepsy and mental retardation." Psychiatric Genetics 18, no. 1 (February 2008): 40–42. http://dx.doi.org/10.1097/ypg.0b013e3282f08a3d.

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Ma, Xiaohong, Jinhua Sun, Jing Yao, Qiang Wang, Xun Hu, Wei Deng, Xueli Sun, et al. "A quantitative association study between schizotypal traits and COMT, PRODH and BDNF genes in a healthy Chinese population." Psychiatry Research 153, no. 1 (September 2007): 7–15. http://dx.doi.org/10.1016/j.psychres.2007.02.003.

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Glaser, Beate, Valentina Moskvina, George Kirov, Kieran C. Murphy, Hywel Williams, Nigel Williams, Michael J. Owen, and Michael C. O'Donovan. "Analysis of ProDH, COMT and ZDHHC8 risk variants does not support individual or interactive effects on schizophrenia susceptibility." Schizophrenia Research 87, no. 1-3 (October 2006): 21–27. http://dx.doi.org/10.1016/j.schres.2006.05.024.

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Kempf, Lucas, Kristin K. Nicodemus, Bhaskar Kolachana, Radhakrishna Vakkalanka, Beth A. Verchinski, Michael F. Egan, Richard E. Straub, et al. "Functional Polymorphisms in PRODH Are Associated with Risk and Protection for Schizophrenia and Fronto-Striatal Structure and Function." PLoS Genetics 4, no. 11 (November 7, 2008): e1000252. http://dx.doi.org/10.1371/journal.pgen.1000252.

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Richard, Anne Claire, Anne Rovelet-Lecrux, Elsa Delaby, Camille Charbonnier, Bhooma Thiruvahindrapuram, Eli Hatchwell, Peggy S. Eis, et al. "The 22q11 PRODH/DGCR6 deletion is frequent in hyperprolinemic subjects but is not a strong risk factor for ASD." American Journal of Medical Genetics Part B: Neuropsychiatric Genetics 171, no. 3 (January 14, 2016): 377–82. http://dx.doi.org/10.1002/ajmg.b.32416.

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Li, Dawei, and Lin He. "Association study of the G-protein signaling 4 (RGS4) and proline dehydrogenase (PRODH) genes with schizophrenia: a meta-analysis." European Journal of Human Genetics 14, no. 10 (June 21, 2006): 1130–35. http://dx.doi.org/10.1038/sj.ejhg.5201680.

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de Koning, Mariken B., Esther D. A. van Duin, Erik Boot, Oswald J. N. Bloemen, Jaap A. Bakker, Kathryn M. Abel, and Thérèse A. M. J. van Amelsvoort. "PRODH rs450046 and proline x COMT Val158Met interaction effects on intelligence and startle in adults with 22q11 deletion syndrome." Psychopharmacology 232, no. 17 (June 12, 2015): 3111–22. http://dx.doi.org/10.1007/s00213-015-3971-5.

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Satoh, Rie, Yasunari Fujita, Kazuo Nakashima, Kazuo Shinozaki, and Kazuko Yamaguchi-Shinozaki. "A Novel Subgroup of bZIP Proteins Functions as Transcriptional Activators in Hypoosmolarity-Responsive Expression of the ProDH Gene in Arabidopsis." Plant and Cell Physiology 45, no. 3 (March 15, 2004): 309–17. http://dx.doi.org/10.1093/pcp/pch036.

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Gellatly, Désirée, Daniela M. Meléndez, Sonia Marti, Diego Moya, Xiaohui Yang, John S. Church, and Karen S. Schwartzkopf-Genswein. "319 Effects of repeated exposure to either energized or non-energized prods on the behavioral responses of beef cattle to handling." Journal of Animal Science 97, Supplement_3 (December 2019): 7. http://dx.doi.org/10.1093/jas/skz258.011.

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Abstract The cattle industry has adopted the use of low stress handling aids however, the continuous-pulse electric prod is still used on hard-to-move cattle. This study aimed to assess behavioral responses of beef cattle after five consecutive exposures to either energized or non-energized prods for 1 s while enclosed in a squeeze chute. A total of 208 7–8 mo old crossbred Angus steers (487.6 ± 41.68 kg BW) were randomly assigned to 1 of 4 treatments: non-energized prod (CT), continuous-pulse electric prod (CP), broken-pulse electric prod (BP) and a vibration prod (VP) that did not produce a shock. Prior to (d -3, -2 and -1; baseline), during (d 0, 1, 2, 3 and 4) and after (d 5, 6 and 7) the application of treatments, behavior of each steer was assessed including: using voice and touch (VAT; score), race transit time (RTT; s), squeeze chute score (SC; score) and flight speed (FS; m/s). Data was analyzed using GLIMMIX procedure of SAS including treatment, day and interaction as fixed effects. No treatment effect (P > 0.05) was found for VAT. The VP steers had greater (P < 0.05) RTT on d 4 and 5 compared to CT and CP, respectively. The CP steers had greater (P < 0.05) SC than CT, BP and VP. The CP had greater (P < 0.05) FS from d 0 to 7 compared to all other treatments with the exception that no differences (P > 0.05) were observed on d 1 between CP and BP. Based on SC and FS, the CP prod was more aversive to cattle than all other prods. However, due to the lack of differences in VAT and RTT measures between control and electric prods, further studies are required to determine the aversiveness of prods balanced with their ability to move hard-to-move cattle.

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Satoh, Rie, Kazuo Nakashima, Motoaki Seki, Kazuo Shinozaki, and Kazuko Yamaguchi-Shinozaki. "ACTCAT, a Novel cis-Acting Element for Proline- and Hypoosmolarity-Responsive Expression of the ProDH Gene Encoding Proline Dehydrogenase in Arabidopsis." Plant Physiology 130, no. 2 (October 1, 2002): 709–19. http://dx.doi.org/10.1104/pp.009993.

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Tunbridge, Elizabeth, Philip W. J. Burnet, Monsheel S. Sodhi, and Paul J. Harrison. "Catechol-o-methyltransferase (COMT) and proline dehydrogenase (PRODH) mRNAs in the dorsolateral prefrontal cortex in schizophrenia, bipolar disorder, and major depression." Synapse 51, no. 2 (2003): 112–18. http://dx.doi.org/10.1002/syn.10286.

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Hayashi, Fumio, Takuya Ichino, Minoru Osanai, and Keishiro Wada. "Oscillation and Regulation of Proline Content by P5CS and ProDH Gene Expressions in the Light/Dark Cycles in Arabidopsis thaliana L." Plant and Cell Physiology 41, no. 10 (October 15, 2000): 1096–101. http://dx.doi.org/10.1093/pcp/pcd036.

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Сергєєва, Л. Є., and Л. І. Броннікова. "PROLINE IN WINTER WHEAT SHOOTS, OBTAINED AFTER GENETIC TRANSFORMATION." Біорізноманіття, екологія та експериментальна біологія, no. 22 (2020): 106–14. http://dx.doi.org/10.34142/2708-5848.2020.22.1.10.

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Gene engineering is one of the most appropriate methods for obtaining plants with higher tolerance to osmotic stresses. Osmotic stress stimulates the synthesis of compatible solutions that protect plants. The free proline was suggested as one of the possible means for overcoming osmotic stress. Its degradation after stress can provide nitrogen, carbon energy. The enzyme connected with proline degradation is proline dehydrogenase, (ProDH). ProDH serves important functions of stress reactions and the development of plants. Agrobacterium-mediated winter wheat transformation in planta using the strain LBA4404 was performed. The primary forms, genotypes UK 95/17 and UK 322/17, were selected in the Institute of Plant Physiology and Genetics of the National Academy of Sciences of Ukraine. The seeds were gathered and considered to be T0 generation, but till the experiment insertions of the transgene were not verified by PCR. The seeds were germinated on filter paper soaked with a 0.5M solution of mannitol. Germination frequencies were scored after a week of incubation. Mannitol affected seed germination in all tested types. At the same time genotype differences were observed. Under stress condition, the germination level of 95/17 initial form exceeded this parameter of T0 variants. At the same time, the 322/17 genotype demonstrated the opposite tendency. To study the salt resistance of the seeds, they were germinated in 0.5 diluted Murashige-Skuga solution with the addition of 20.0 g / l of seawater salts for 10 days. Free proline levels were estimated in the leaves of 10-day shoots. The winter wheat genotypes demonstrated peculiar characteristics. Salinity provoked the growth of free proline levels. For initial forms of UK95/17 and UK322/17, the proline levels were 1.77 and 4.53 times higher than normal parameters. At the same time under salinity the proline levels in T0 shoots of genotype 95/17 were 0.28–1.43 times and in T0 shoots of genotype 322/17 were 2.67–3.70 times of control marks. However, the proline numerical data of T0 forms of both genotypes were lower than the stress figures of their initial forms. Under osmotic stresses, the increase of proline is usually due to the growth of its synthesis. The events of transgene insertions were not verified by PCR. So we have no open data about transgene activity. But the peculiar features that we observed can be indicators of the indirect influence of transgene. The plant proline level even under normal conditions is not a constant feature but it changes during the vegetation. Proline is not only a compatible osmolyte but regulates the gene expression. In our opinion, the effectiveness of such a construction for obtaining plant forms with higher stress tolerance can be estimated during changes in stress/restoration conditions.

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