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https://www.readbyqxmd.com/read/29321346/mutational-screening-of-pkd2-gene-in-the-north-indian-polycystic-kidney-disease-patients-revealed-28-genetic-variations
#1
Sonam Raj, Rana Gopal Singh, Parimal Das
Polycystic kidney disease (PKD) is a systemic disorder which adds majority of renal patients to end stage renal disease. Autosomal dominant polycystic kidney disease (ADPKD) is more prevalent and leading cause of dialysis and kidney transplant. Linkage analysis revealed some closely linked loci, two of which are identified as PKD1, PKD2 and an unidentified locus to ADPKD. This study was performed using PCR and automated DNA sequencing in 84 cases and 80 controls to test potential candidature of PKD2 as underlying cause of PKD by in silico and statistical analyses...
December 2017: Journal of Genetics
https://www.readbyqxmd.com/read/29306517/patterns-of-kidney-function-decline-in-autosomal-dominant-polycystic-kidney-disease-a-post-hoc-analysis-from-the-halt-pkd-trials
#2
Godela M Brosnahan, Kaleab Z Abebe, Charity G Moore, Frederic F Rahbari-Oskoui, Kyongtae T Bae, Jared J Grantham, Robert W Schrier, William E Braun, Arlene B Chapman, Michael F Flessner, Peter C Harris, Marie C Hogan, Ronald D Perrone, Dana C Miskulin, Theodore I Steinman, Vicente E Torres
BACKGROUND: Previous clinical studies of autosomal dominant polycystic kidney disease (ADPKD) reported that loss of kidney function usually follows a steep and relentless course. A detailed examination of individual patterns of decline in estimated glomerular filtration rate (eGFR) has not been performed. STUDY DESIGN: Longitudinal post hoc analysis of data collected during the Halt Progression of Polycystic Kidney Disease (HALT-PKD) trials. SETTING & PARTICIPANTS: 494 HALT-PKD Study A participants (younger; preserved eGFR) and 435 Study B participants (older; reduced eGFR) who had more than 3 years of follow-up and 7 or more eGFR assessments...
January 3, 2018: American Journal of Kidney Diseases: the Official Journal of the National Kidney Foundation
https://www.readbyqxmd.com/read/29273751/excitotoxic-inactivation-of-constitutive-oxidative-stress-detoxification-pathway-in-neurons-can-be-rescued-by-pkd1
#3
Julia Pose-Utrilla, Lucía García-Guerra, Ana Del Puerto, Abraham Martín, Jerónimo Jurado-Arjona, Noelia S De León-Reyes, Andrea Gamir-Morralla, Álvaro Sebastián Serrano, Mónica García-Gallo, Leonor Kremer, Jens Fielitz, Christofer Ireson, Mª José Pérez-Álvarez, Isidro Ferrer, Félix Hernández, Jesús Ávila, Marina Lasa, Miguel R Campanero, Teresa Iglesias
Excitotoxicity, a critical process in neurodegeneration, induces oxidative stress and neuronal death through mechanisms largely unknown. Since oxidative stress activates protein kinase D1 (PKD1) in tumor cells, we investigated the effect of excitotoxicity on neuronal PKD1 activity. Unexpectedly, we find that excitotoxicity provokes an early inactivation of PKD1 through a dephosphorylation-dependent mechanism mediated by protein phosphatase-1 (PP1) and dual specificity phosphatase-1 (DUSP1). This step turns off the IKK/NF-κB/SOD2 antioxidant pathway...
December 22, 2017: Nature Communications
https://www.readbyqxmd.com/read/29259300/protein-kinase-d2-a-versatile-player-in-cancer-biology
#4
REVIEW
Ninel Azoitei, Mathias Cobbaut, Alexander Becher, Johan Van Lint, Thomas Seufferlein
Protein kinase D2 (PKD2) is a serine/threonine kinase that belongs to the PKD family of calcium-calmodulin kinases, which comprises three isoforms: PKD1, PKD2, and PKD3. PKD2 is activated by many stimuli including growth factors, phorbol esters, and G-protein-coupled receptor agonists. PKD2 participation to uncontrolled growth, survival, neovascularization, metastasis, and invasion has been documented in various tumor types including pancreatic, colorectal, gastric, hepatic, lung, prostate, and breast cancer, as well as glioma multiforme and leukemia...
December 20, 2017: Oncogene
https://www.readbyqxmd.com/read/29225991/administration-of-protein-kinase-d1-induces-a-protective-effect-on-lipopolysaccharide-induced-intestinal-inflammation-in-a-co-culture-model-of-intestinal-epithelial-caco-2-cells-and-raw264-7-macrophage-cells
#5
Ditte Søvsø Gundelund Nielsen, Marlene Fredborg, Vibeke Andersen, Stig Purup
Inflammatory bowel diseases (IBD) are chronic inflammatory diseases involving all or part of the gastrointestinal tract. The stress-activated serine-threonine protein kinase D1 (PKD1) protein has previously been implicated in intestinal immune regulation. The objective of this study was to evaluate the effects of human PKD1 in relation to intestinal inflammation, using a co-culture model of intestinal epithelial Caco-2 cells and RAW264.7 macrophages. An inflammatory response was induced in the macrophages by lipopolysaccharide (LPS), upregulating the expression of tumour necrosis factor alpha (TNF-α), interleukin- (IL-) 1β, and IL-6 besides increasing the secretion of TNF-α protein...
2017: International Journal of Inflammation
https://www.readbyqxmd.com/read/29218111/the-diagnostic-value-of-microrna-4787-5p-and-microrna-4306-in-patients-with-acute-aortic-dissection
#6
Lei Wang, Shijie Zhang, Zhigao Xu, Jingjing Zhang, Li Li, Guoqiang Zhao
Acute aortic dissection (AAD) is a life-threatening cardiovascular disease with the high morbidity and mortality. Imaging modalities are the gold standard for the diagnosis of AAD; however, they are not always available in emergency department. Biomarker-assisted diagnosis is important for the early treatment of AAD. The aim of the present study was to identify potential microRNA (miRNA) biomarkers for AAD. Differentially expressed plasma miRNAs between AAD patients and age-matched healthy volunteers were analyzed by miRNA microarray...
2017: American Journal of Translational Research
https://www.readbyqxmd.com/read/29211809/down-regulation-of-the-klf5-c-myc-interaction-due-to-klf5-phosphorylation-mediates-resveratrol-repressing-the-caveolin-1-transcription-through-the-pi3k-pkd1-akt-pathway
#7
Hui Yang, Qiuxia Chen, Fangyun Sun, Nana Zhao, Lirong Wen, Lin Li, Gai Ran
Resveratrol (RSV), a natural polyphenol, has been reported to produce effect on genes transcription in lipid metabolism. In this study, we aim to explore the novel mechanisms of RSV on the regulation of caveolin-1 (Cav-1) transcription. Via body weight, blood glucose, serum lipid, and liver pathology detection, we found that RSV decreased body weight, blood glucose and lipid accumulation in rats fed high-fat diet. Based on co-immunoprecipitation (Co-IP) and western blotting assay, we found that RSV up-regulated klf5 phosphorylation and decreased the interaction of klf5 with c-Myc, which were accompanied by down-regulation of Cav-1 expression in livers of rats fed with high-fat diet...
2017: PloS One
https://www.readbyqxmd.com/read/29202470/polycystin-1-interacts-with-taz-to-stimulate-osteoblastogenesis-and-inhibit-adipogenesis
#8
Zhousheng Xiao, Jerome Baudry, Li Cao, Jinsong Huang, Hao Chen, Charles R Yates, Wei Li, Brittany Dong, Christopher M Waters, Jeremy C Smith, L Darryl Quarles
The molecular mechanisms that transduce the osteoblast response to physical forces in the bone microenvironment are poorly understood. Here, we used genetic and pharmacological experiments to determine whether the polycystins PC1 and PC2 (encoded by Pkd1 and Pkd2) and the transcriptional coactivator TAZ form a mechanosensing complex in osteoblasts. Compound-heterozygous mice lacking 1 copy of Pkd1 and Taz exhibited additive decrements in bone mass, impaired osteoblast-mediated bone formation, and enhanced bone marrow fat accumulation...
November 27, 2017: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/29133434/pkd1-promotes-functional-synapse-formation-coordinated-with-n-cadherin-in-hippocampus
#9
Cheng Cen, Li-Da Luo, Wen-Qi Li, Gang Li, Na-Xi Tian, Ge Zheng, Dong-Min Yin, Yimin Zou, Yun Wang
Functional synapse formation is critical for the wiring of neural circuits in the developing brain. The cell adhesion molecule N-cadherin plays important roles in target recognition and synaptogenesis. However, the molecular mechanisms that regulate the localization of N-cadherin and the subsequent effects remain poorly understood. Here, we show that protein kinase D1 (PKD1) directly binds to N-cadherin at amino acid residues 836-871 and phosphorylates it at Ser 869, 871, 872, thereby increasing the surface localization of N-cadherin and promoting functional synapse formation in primary cultured hippocampal neurons obtained from embryonic day 18 rat embryos of either sex...
November 13, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/29121521/induced-pluripotent-stem-cells-derived-from-an-autosomal-dominant-polycystic-kidney-disease-patient-carrying-a-pkd1-q533x-mutation
#10
Jia-Jung Lee, Ming-Ching Ho, Ching-Ying Huang, Cheng-Hao Wen, Yu-Che Cheng, Yu-Hung Hsu, Daw-Yang Hwang, Huai-En Lu, Hung-Chun Chen, Patrick C H Hsieh
Autosomal Dominant Polycystic Kidney Disease (ADPKD) is the most prevalent monogenic kidney disorder leading to kidney failure. We generated induced pluripotent stem cells (iPSCs) from a 37-year-old man carrying a PKD1 Q533X mutation who suffered from kidney failure and a myocardial infarction. The iPSCs were reprogrammed from the patient's peripheral blood mononuclear cells using the Sendai virus system, and were confirmed to possess the specific PKD1 Q533X mutation and normal karyotype. Pluripotency was confirmed using in vitro and in vivo assays...
October 28, 2017: Stem Cell Research
https://www.readbyqxmd.com/read/29107072/ectopic-phosphorylated-creb-marks-dedifferentiated-proximal-tubules-in-cystic-kidney-disease
#11
Pawan Puri, Caitlin M Schaefer, Daniel Bushnell, Mary E Taglienti, Jordan A Kreidberg, Bradley K Yoder, Carlton M Bates
Ectopic cAMP signaling is pathological in polycystic kidney disease; however, its spatio-temporal actions are unclear. We characterized expression of phosphorylated Creb (p-Creb), a target and mediator of cAMP signaling, in developing and cystic kidney models. We also examined tubule-specific effects of cAMP analogs in cystogenesis in embryonic kidney explants. In wild-type mice, p-Creb marked nephron progenitors (NP), early epithelial NP derivatives, ureteric bud, and cortical stroma; p-Creb was present in differentiated thick ascending limb of Henle, collecting duct, and stroma; however, it disappeared in mature NP-derived proximal tubules...
October 26, 2017: American Journal of Pathology
https://www.readbyqxmd.com/read/29074972/profiling-of-mirnas-and-target-genes-related-to-cystogenesis-in-adpkd-mouse-models
#12
Yu Mi Woo, Do Yeon Kim, Nam Jin Koo, Yong-Min Kim, Sunyoung Lee, Je Yeong Ko, Yubin Shin, Bo Hye Kim, Hyowon Mun, Seonju Choi, Eun Ji Lee, Jeong-Oh Shin, Eun Young Park, Jinwoong Bok, Jong Hoon Park
Autosomal polycystic kidney disease (ADPKD) is a common inherited renal disease characterized by the development of numerous fluid-filled cysts in both kidneys. We investigated miRNA-mediated regulatory systems and networks that play an important role during cystogenesis through integrative analysis of miRNA- and RNA-seq using two ADPKD mouse models (conditional Pkd1- or Pkd2-deficient mice), at three different time points (P1, P3, and P7). At each time point, we identified 13 differentially expressed miRNAs (DEmiRs) and their potential targets in agreement with cyst progression in both mouse models...
October 26, 2017: Scientific Reports
https://www.readbyqxmd.com/read/29063115/-trpv1-an-important-molecule-involved-in-the-peripheral-sensitization-during-chronic-pain-and-central-pain-modulation
#13
Ying Zhang, Yun Wang
As chronic pain is a severe problem in clinics, study of the mechanisms of chronic pain and development of novel analgesic agents is of significance. In the past decade, our lab completed a series of studies on the regulatory mechanisms of functional sensitization and membrane trafficking of transient receptor potential vanilloid type 1 (TRPV1), a key molecule involved in the development of peripheral sensitization. Our studies elucidated the important regulatory roles of several protein kinases, including PKD1 (protein kinase D1), Cdk5 (cyclin-dependent kinase 5) and LIMK (LIM-motif containing kinase), in inflammatory thermal hyperalgesia...
October 25, 2017: Sheng Li Xue Bao: [Acta Physiologica Sinica]
https://www.readbyqxmd.com/read/29058231/computational-design-of-new-protein-kinase-d-1-pkd1-inhibitors-homology-based-active-site-prediction-energy-optimized-pharmacophore-docking-and-database-screening
#14
Nalini, Navriti Chadha, Malkeet Singh Bahia, Maninder Kaur, Renu Bahadur, Om Silakari
Protein kinase D 1 (PKD1) overexpression has a well-validated role in cancer progression and its inhibitors have defined a protective role-play of PKD1 for various cancers such as prostate, pancreatic and noninvasive breast cancers, and more. Therefore, the current research was aimed at designing new PKD1 inhibitors combining different ligand- and structure-based computational drug designing methodologies. Initially, the three-dimensional structure of PKD1's active site was computationally modeled, corrected using molecular dynamic simulations and validated for docking experiments...
October 23, 2017: Molecular Diversity
https://www.readbyqxmd.com/read/29038309/deletion-of-protein-kinase-d1-in-pancreatic-beta-cells-impairs-insulin-secretion-in-high-fat-fed-mice
#15
Valérie Bergeron, Julien Ghislain, Kevin Vivot, Natalia Tamarina, Louis H Philipson, Jens Fielitz, Vincent Poitout
Beta-cell adaptation to insulin resistance is necessary to maintain glucose homeostasis in obesity. Failure of this mechanism is a hallmark of type 2 diabetes (T2D). Hence, factors controlling functional beta-cell compensation are potentially important targets for the treatment of T2D. Protein kinase D1 (PKD1) integrates diverse signals in the beta cell and plays a critical role in the control of insulin secretion. However, the role of beta-cell PKD1 in glucose homeostasis in vivo is essentially unknown. Using beta-cell specific, inducible PKD1 knock-out mice (βPKD1KO), we examined the role of beta-cell PKD1 under basal conditions and during high-fat feeding...
October 16, 2017: Diabetes
https://www.readbyqxmd.com/read/29038287/genetic-complexity-of-autosomal-dominant-polycystic-kidney-and-liver-diseases
#16
Emilie Cornec-Le Gall, Vicente E Torres, Peter C Harris
Data indicate significant phenotypic and genotypic overlap, plus a common pathogenesis, between two groups of inherited disorders, autosomal dominant polycystic kidney diseases (ADPKD), a significant cause of ESRD, and autosomal dominant polycystic liver diseases (ADPLD), which result in significant PLD with minimal PKD. Eight genes have been associated with ADPKD (PKD1 and PKD2), ADPLD (PRKCSH, SEC63, LRP5, ALG8, and SEC61B), or both (GANAB). Although genetics is only infrequently used for diagnosing these diseases and prognosing the associated outcomes, its value is beginning to be appreciated, and the genomics revolution promises more reliable and less expensive molecular diagnostic tools for these diseases...
January 2018: Journal of the American Society of Nephrology: JASN
https://www.readbyqxmd.com/read/29035198/affected-parent-sex-and-severity-of-autosomal-dominant-polycystic-kidney-disease-a-retrospective-cohort-study%C3%A2
#17
Kristen L Nowak, Michel Chonchol, Zhiying You, Malika Gupta, Berenice Gitomer
OBJECTIVE: Parental inheritance may differentially affect autosomal dominant polycystic kidney disease (-ADPKD) severity via genetic imprinting or in utero epigenetic modifications; however, evidence is inconsistent. We conducted a longitudinal retrospective cohort study to assess the association between sex of the affected parent and time to hypertension diagnosis, end-stage renal disease (ESRD), and death in patients with the PKD1 genotype. MATERIALS AND METHODS: 814 individuals who participated in research at the University of Colorado were studied...
October 16, 2017: Clinical Nephrology
https://www.readbyqxmd.com/read/29034881/generation-of-induced-pluripotent-stem-cells-derived-from-an-autosomal-dominant-polycystic-kidney-disease-patient-with-a-p-ser1457fs-mutation-in-pkd1
#18
Ching-Ying Huang, Ming-Ching Ho, Jia-Jung Lee, Daw-Yang Hwang, Hui-Wen Ko, Yu-Che Cheng, Yu-Hung Hsu, Huai-En Lu, Hung-Chun Chen, Patrick C H Hsieh
Autosomal dominant polycystic kidney disease is one of the most prevalent forms of inherited cystic kidney disease, and can be characterized by kidney cyst formation and enlargement. Here we report the generation of a Type 1 ADPKD disease iPS cell line, IBMS-iPSC-012-12, which retains the conserved deletion of PKD1, normal karyotype and exhibits the properties of pluripotent stem cells such as ES-like morphology, expression of pluripotent markers and capacity to differentiate into all three germ layers. Our results show that we have successfully generated a patient-specific iPS cell line with a mutation in PKD1 for study of renal disease pathophysiology...
October 2017: Stem Cell Research
https://www.readbyqxmd.com/read/29026418/heterozygosity-analysis-of-polycystic-kidney-disease-1-gene-microsatellite-markers-for-linkage-analysis-of-autosomal-dominant-polycystic-kidney-disease-type-1-in-the-iranian-population
#19
Razieh Fatehi, Sharifeh Khosravi, Maryam Abedi, Rasoul Salehi, Yousof Gheisari
BACKGROUND: Autosomal dominant polycystic kidney disease (ADPKD) is the most common genetic cause of end-stage renal disease. Although imaging techniques are a means of accurate diagnosis when the cysts appear in the third or fourth decades of the patient's life, they are of little value for early diagnosis. Genetic tests are required for preimplantation genetic diagnosis, decision-making for kidney donation to an affected relative. Although mutation of the polycystic kidney disease (PKD1) gene is solely responsible for the most cases of ADPKD, direct genetic testing is limited by the large size of this gene and the presence of many mutations without hot spots...
2017: Journal of Research in Medical Sciences: the Official Journal of Isfahan University of Medical Sciences
https://www.readbyqxmd.com/read/29021226/attenuation-of-accelerated-renal-cystogenesis-in-pkd1-mice-by-renin-angiotensin-system-blockade
#20
Wayne R Fitzgibbon, Yujing Dang, Marlene A Bunni, Catalin F Baicu, Michael R Zile, Adam E Mullick, Takamitsu Saigusa
BACKGROUND: The intrarenal renin angiotensin system (RAS) is activated in polycystic kidney disease. We have recently shown in the Pkd1 mouse that Gen 2 antisense oligonucleotide (ASO), which suppresses angiotensinogen (Agt) synthesis, is efficacious in slowing kidney cyst formation compared to lisinopril. The aim of this current study was to determine 1) if unilateral nephrectomy accelerates cystogenesis in Pkd1 mice (as previously shown in cilia knockout mice), and 2) whether Agt ASO can slow the progression in this accelerated cystic mouse model...
October 11, 2017: American Journal of Physiology. Renal Physiology
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