Relevant bibliographies by topics / DDAH2

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'DDAH2'

Author: Grafiati
Published: 2 June 2025
Last updated: 31 July 2025

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'DDAH2.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "DDAH2"

1

Kozlova, Alena A., Anastasia N. Vaganova, Roman N. Rodionov, Raul R. Gainetdinov, and Nadine Bernhardt. "Assessment of DDAH1 and DDAH2 Contributions to Psychiatric Disorders via In Silico Methods." International Journal of Molecular Sciences 23, no. 19 (2022): 11902. http://dx.doi.org/10.3390/ijms231911902.

Full text
Abstract:
The contribution of nitric oxide synthases (NOSs) to the pathophysiology of several neuropsychiatric disorders is recognized, but the role of their regulators, dimethylarginine dimethylaminohydrolases (DDAHs), is less understood. This study’s objective was to estimate DDAH1 and DDAH2 associations with biological processes implicated in major psychiatric disorders using publicly accessible expression databases. Since co-expressed genes are more likely to be involved in the same biologic processes, we investigated co-expression patterns with DDAH1 and DDAH2 in the dorsolateral prefrontal cortex
APA, Harvard, Vancouver, ISO, and other styles
2

Dayal, Sanjana, Roman N. Rodionov, Erland Arning, et al. "Tissue-specific downregulation of dimethylarginine dimethylaminohydrolase in hyperhomocysteinemia." American Journal of Physiology-Heart and Circulatory Physiology 295, no. 2 (2008): H816—H825. http://dx.doi.org/10.1152/ajpheart.01348.2007.

Full text
Abstract:
Asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide (NO) synthase, has been proposed to be a mediator of vascular dysfunction during hyperhomocysteinemia. Levels of ADMA are regulated by dimethylarginine dimethylaminohydrolase (DDAH). Using both in vitro and in vivo approaches, we tested the hypothesis that hyperhomocysteinemia causes downregulation of the two genes encoding DDAH ( Ddah1 and Ddah2). In the MS-1 murine endothelial cell line, the addition of homocysteine decreased NO production but did not elevate ADMA or alter levels of Ddah1 or Ddah2 mRNA. Mice heterozy
APA, Harvard, Vancouver, ISO, and other styles
3

Ivashchenko, Christine Y., Benjamin T. Bradley, Zhaohui Ao, James Leiper, Patrick Vallance, and Douglas G. Johns. "Regulation of the ADMA-DDAH system in endothelial cells: a novel mechanism for the sterol response element binding proteins, SREBP1c and -2." American Journal of Physiology-Heart and Circulatory Physiology 298, no. 1 (2010): H251—H258. http://dx.doi.org/10.1152/ajpheart.00195.2009.

Full text
Abstract:
Asymmetric dimethylarginine (ADMA) has been implicated in the progression of cardiovascular disease as an endogenous inhibitor of nitric oxide synthase. The regulation of dimethylarginine dimethylaminohydrolase (DDAH), the enzyme responsible for metabolizing ADMA, is poorly understood. The transcription factor sterol response element binding protein (SREBP) is activated by statins via a reduction of membrane cholesterol content. Because the promoters of both DDAH1 and DDAH2 isoforms contain sterol response elements, we tested the hypothesis that simvastatin regulates DDAH1 and DDAH2 transcript
APA, Harvard, Vancouver, ISO, and other styles
4

Sasaki, Akihito, Shouzaburoh Doi, Shuki Mizutani, and Hiroshi Azuma. "Roles of accumulated endogenous nitric oxide synthase inhibitors, enhanced arginase activity, and attenuated nitric oxide synthase activity in endothelial cells for pulmonary hypertension in rats." American Journal of Physiology-Lung Cellular and Molecular Physiology 292, no. 6 (2007): L1480—L1487. http://dx.doi.org/10.1152/ajplung.00360.2006.

Full text
Abstract:
Nitric oxide (NO) has been suggested to play a key role in the pathogenesis of pulmonary hypertension (PH). To determine which mechanism exists to affect NO production, we examined the concentration of endogenous nitric oxide synthase (NOS) inhibitors and their catabolizing enzyme dimethylarginine dimethylaminohydrolase (DDAH) activity and protein expression (DDAH1 and DDAH2) in pulmonary artery endothelial cells (PAECs) of rats given monocrotaline (MCT). We also measured NOS and arginase activities and NOS protein expression. Twenty-four days after MCT administration, PH and right ventricle (
APA, Harvard, Vancouver, ISO, and other styles
5

Hannemann, Juliane, Patricia Siques, Lena Schmidt-Hutten, Julia Zummack, Julio Brito, and Rainer Böger. "Association of Genes of the NO Pathway with Altitude Disease and Hypoxic Pulmonary Hypertension." Journal of Clinical Medicine 10, no. 24 (2021): 5761. http://dx.doi.org/10.3390/jcm10245761.

Full text
Abstract:
Chronic intermittent hypoxia leads to high-altitude pulmonary hypertension, which is associated with high asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthesis. Therefore, we aimed to understand the relation of single nucleotide polymorphisms in this pathway to high-altitude pulmonary hypertension (HAPH). We genotyped 69 healthy male Chileans subjected to chronic intermittent hypoxia. Acclimatization to altitude was determined using the Lake Louise Score and the presence of acute mountain sickness. Echocardiography was performed after six months in 24 individual
APA, Harvard, Vancouver, ISO, and other styles
6

Krzystek-Korpacka, Małgorzata, Berenika Szczęśniak-Sięga, Izabela Szczuka, et al. "L-Arginine/Nitric Oxide Pathway Is Altered in Colorectal Cancer and Can Be Modulated by Novel Derivatives from Oxicam Class of Non-Steroidal Anti-Inflammatory Drugs." Cancers 12, no. 9 (2020): 2594. http://dx.doi.org/10.3390/cancers12092594.

Full text
Abstract:
L-arginine/nitric oxide pathway metabolites are altered in colorectal cancer (CRC). We evaluated underlying changes in pathway enzymes in 55 paired tumor/tumor-adjacent samples and 20 normal mucosa using quantitative-PCR and assessed the impact of classic and novel oxicam analogues on enzyme expression and intracellular metabolite concentration (LC-MS/MS) in Caco-2, HCT116, and HT-29 cells. Compared to normal mucosa, ARG1, PRMT1, and PRMT5 were overexpressed in both tumor and tumor-adjacent tissue and DDAH2 solely in tumor-adjacent tissue. Tumor-adjacent tissue had higher expression of ARG1, D
APA, Harvard, Vancouver, ISO, and other styles
7

Hannemann, Juliane, Julia Zummack, Jonas Hillig, Leonard Rendant-Gantzberg, and Rainer Böger. "Association of Variability in the DDAH1, DDAH2, AGXT2 and PRMT1 Genes with Circulating ADMA Concentration in Human Whole Blood." Journal of Clinical Medicine 11, no. 4 (2022): 941. http://dx.doi.org/10.3390/jcm11040941.

Full text
Abstract:
Asymmetric dimethylarginine is an endogenous inhibitor of nitric oxide synthesis and a cardiovascular risk factor. Its regulation has been studied extensively in experimental models, but less in humans. We studied common single-nucleotide polymorphisms (SNPs) in genes encoding for enzymes involved in ADMA biosynthesis and metabolism, i.e., PRMT1, DDAH1, DDAH2, and AGXT2, and assessed their associations with blood ADMA concentration in 377 unselected humans. The minor allele of DDAH1 SNP rs233112 was significantly more frequent in individuals with ADMA in the highest tertile or in the highest q
APA, Harvard, Vancouver, ISO, and other styles
8

Wang, Zhong, Shaoze Chen, Lina Zhang, et al. "Association between variation in the genes DDAH1 and DDAH2 and hypertension among Uygur, Kazakh and Han ethnic groups in China." Sao Paulo Medical Journal 134, no. 3 (2016): 205–10. http://dx.doi.org/10.1590/1516-3180.2015.01150108.

Full text
Abstract:
CONTEXT AND OBJECTIVE: Dimethylarginine dimethylaminohydrolase enzymes (DDAH), which are encoded by the genes DDAH1 and DDAH2, play a fundamental role in maintaining endothelial function. We conducted a case-control study on a Chinese population that included three ethnic groups (Han, Kazakh and Uygur), to systemically investigate associations between variations in the genes DDAH1 and DDAH2 and hypertension. DESIGN AND SETTING: Experimental study at the Department of Internal Medicine and Genetic Diagnosis, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology.
APA, Harvard, Vancouver, ISO, and other styles
9

Krzystek-Korpacka, Małgorzata, Mariusz G. Fleszar, Iwona Bednarz-Misa, et al. "Transcriptional and Metabolomic Analysis of L-Arginine/Nitric Oxide Pathway in Inflammatory Bowel Disease and Its Association with Local Inflammatory and Angiogenic Response: Preliminary Findings." International Journal of Molecular Sciences 21, no. 5 (2020): 1641. http://dx.doi.org/10.3390/ijms21051641.

Full text
Abstract:
L-arginine/nitric oxide pathway in Crohn’s disease (CD) and ulcerative colitis (UC) is poorly investigated. The aim of current study is to quantify pathway serum metabolites in 52 CD (40 active), 48 UC (33 active), and 18 irritable bowel syndrome patients and 40 controls using mass spectrometry and at determining mRNA expression of pathway-associated enzymes in 91 bowel samples. Arginine and symmetric dimethylarginine decreased (p < 0.05) in active-CD (129 and 0.437 µM) compared to controls (157 and 0.494 µM) and active-UC (164 and 0.52 µM). Citrulline and dimethylamine increased (p < 0.
APA, Harvard, Vancouver, ISO, and other styles
10

Jarzebska, Natalia, Arduino A. Mangoni, Jens Martens-Lobenhoffer, Stefanie M. Bode-Böger, and Roman N. Rodionov. "The Second Life of Methylarginines as Cardiovascular Targets." International Journal of Molecular Sciences 20, no. 18 (2019): 4592. http://dx.doi.org/10.3390/ijms20184592.

Full text
Abstract:
Endogenous methylarginines were proposed as cardiovascular risk factors more than two decades ago, however, so far, this knowledge has not led to the development of novel therapeutic approaches. The initial studies were primarily focused on the endogenous inhibitors of nitric oxide synthases asymmetric dimethylarginine (ADMA) and monomethylarginine (MMA) and the main enzyme regulating their clearance dimethylarginine dimethylaminohydrolase 1 (DDAH1). To date, all the screens for DDAH1 activators performed with the purified recombinant DDAH1 enzyme have not yielded any promising hits, which is
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "DDAH2"

1

Kelly, P. D. "Elucidation of the biochemical and physiological role of DDAH2." Thesis, University College London (University of London), 2011. http://discovery.ucl.ac.uk/1317766/.

Full text
Abstract:
The asymmetric methylarginines monomethyl-L-arginine (L-NMMA) and asymmetric dimethylarginine (ADMA) are endogenously occurring inhibitors of the nitric oxide synthase (NOS) enzymes. Elevated plasma ADMA has been identified in a range of human cardiovascular disorders, some of which are associated with impaired NO signaling. The dimethylarginine dimethlyaminohydrolase (DDAH) enzymes are responsible for the degradation of asymmetric methylarginines in vivo. The physiological link between DDAH, ADMA, and NOS was demonstrated by a mouse genetic knockout of DDAH1. Ddah1+/- mice had elevated ADMA c
APA, Harvard, Vancouver, ISO, and other styles
2

Tran, Cam Thanh Lucy. "Molecular analysis of human DDAH genes." Thesis, University College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.408021.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Tommasi, Sara. "Design and synthesis of human dimethylarginine dimethylaminohydrolase (DDAH) inhibitors and development of a novel DDAH activity assay." Thesis, University of Aberdeen, 2015. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=227616.

Full text
Abstract:
Nitric oxide (NO) is a key physiological messenger, but an excessive production of this molecule can be detrimental, leading to the onset or worsening of many pathological conditions. Dimethylarginine dimethylaminohydrolase (DDAH) is a key enzyme in the NO pathway, involved in the metabolism of asymmetric dimethylarginine (ADMA) and monomethyl arginine (L-NMMA), which are both endogenous inhibitors of NO synthesis. Two isoforms of DDAH have been identified in humans, namely DDAH-1 and DDAH-2. DDAH inhibition represents a promising strategy in the treatment of NO overproduction under pathologic
APA, Harvard, Vancouver, ISO, and other styles
4

Pullamsetti, Soni. "Role of Dimethylarginine Dimethylaminohydrolases (DDAH) in pulmonary arterial hypertension." Giessen VVB Laufersweiler, 2006. http://geb.uni-giessen.de/geb/volltexte/2006/2892/index.html.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Tomlinson, James. "The role of DDAH and ADMA in kidney disease." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/24541.

Full text
Abstract:
Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide (NO) synthesis and elevated plasma levels associate with poor cardiovascular and renal outcomes. The dimethylarginine dimethylaminohydrolase enzymes (DDAHs; 1 and 2) metabolise ADMA. A DDAH1 gene variant associates with higher kidney tissue mRNA expression, lower plasma ADMA but counter-intuitively, a steeper rate of eGFR decline. This indicates that renal DDAH1 activity may be deleterious and circulating ADMA does not necessarily reflect the NO-ADMA balance (or severity of disease) within kidney tissue. This study t
APA, Harvard, Vancouver, ISO, and other styles
6

Dowsett, Laura Bethany. "The role of the NOS-ADMA-DDAH1 pathway in adipocytes and obesity." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/24709.

Full text
Abstract:
Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthase (NOS) which is metabolised by two isoforms of the enzyme dimethylarginine dimethylaminohydrolase (DDAH). Inhibition of DDAH has been shown to increase ADMA concentrations both in vitro and in vivo. Clinically, high concentrations of ADMA have been associated with a range of diseases, particularly cardiovascular disease and more recently obesity. The role of the NO-ADMA-DDAH pathway has not yet been studied in adipose tissue. This thesis sets out to investigate the effects of pathological ADMA exposure firstl
APA, Harvard, Vancouver, ISO, and other styles
7

Pullamsetti, Soni [Verfasser]. "Role of dimethylarginine dimethylaminohydrolases (DDAH) in pulmonary arterial hypertension / vorgelegt von Soni Pullamsetti." Giessen : VVB Laufersweiler, 2006. http://d-nb.info/98866240X/34.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Khanom, N. "Evaluation of novel arginine based inhibitors of DDAH and investigations into radical hydroacylation of vinyl sulfonates." Thesis, University College London (University of London), 2010. http://discovery.ucl.ac.uk/192842/.

Full text
Abstract:
The thesis is in two main sections. In the first section, studies on methylarginine processing enzymes are presented. Dimethyalrginine dimethylaminohydrolase (DDAH) is a class of enzymes involved in the metabolism of methylarginines ADMA and L-NMMA, which indirectly regulate physiological nitric oxide levels. It is desirable to inhibit excess NO in pathological situations, and the arginine mimetic L-257 is a DDAH inhibitor which reduces levels of NO. Synthesis of ester analogues of L-257 proved to be troublesome with a low yielding key guanidine forming reaction. However, amide analogues were
APA, Harvard, Vancouver, ISO, and other styles
9

Sonnenberg, Derek M. "Design and Synthesis of Novel Chloroacetimidine Inactivators as Potential in vivo Activity Probes of DDAH-1 for Regulation of NOS." Thesis, Southern Illinois University at Edwardsville, 2018. http://pqdtopen.proquest.com/#viewpdf?dispub=10247909.

Full text
Abstract:
<p> Nitric Oxide, NO, is an important neurotransmitter and signaling molecule in almost every system of the human body. Its regulation is equally important as a dysfunction in regulation leads to pathophysiologic conditions and disease states. There are many ways that NO is regulated, but one of the more common methods is to regulate the enzyme that creates it, Nitric Oxide Synthases or NOS. Again, many ways to regulate this enzyme exist, but this work focuses on inhibition by an endogenous molecule produced via the normal process of protein degradation, Asymmetric Dimethyl Arginine or ADMA. A
APA, Harvard, Vancouver, ISO, and other styles
10

Bernges, Isabel [Verfasser], and Elke [Akademischer Betreuer] Oetjen. "Die Metabolisierung der Dimethylarginine durch die Enzyme AGXT2 und DDAH1 und deren Anwendung für den Prozess der Drug Discovery / Isabel Bernges. Betreuer: Elke Oetjen." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2014. http://d-nb.info/1064076769/34.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "DDAH2"

1

Desorden de Deficit de Atencion - DDAH. Publicaciones Puertorriquenas, 2006.

Find full text
APA, Harvard, Vancouver, ISO, and other styles

Book chapters on the topic "DDAH2"

1

Bahadoran, Zahra, Mattias Carlström, Parvin Mirmiran, and Asghar Ghasemi. "Asymmetrical Dimethyl Arginine, Nitric Oxide, and Type 2 Diabetes." In The Role of Nitric Oxide in Type 2 Diabetes. BENTHAM SCIENCE PUBLISHERS, 2022. http://dx.doi.org/10.2174/9789815079814122010007.

Full text
Abstract:
Asymmetric dimethylarginine (ADMA), an endogenous competitive inhibitor of nitric oxide (NO) synthase (NOS) isoenzymes, can substantially inhibit vascular NO production at concentrations that are observed in pathophysiological conditions. Over-production of ADMA (via overexpression and/or activity of class 1 of the protein arginine methyltransferases, PRMT-1) alongside decreased catabolism (due to decreased expression and/or activity of dimethylarginine dimethyloaminohydrolase, DDAH) in type 2 diabetes (T2D) and insulin resistance results in increased circulatory and intracellular ADMA levels.
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "DDAH2"

1

Parida, Sasmita, Devpriya Panda, Jyoti Prakash Dash, and Suvendu Chandan Nayak. "Study of DDAP2 for memory allocation in cloud computing." In 2014 International Conference on High Performance Computing and Applications (ICHPCA). IEEE, 2014. http://dx.doi.org/10.1109/ichpca.2014.7045297.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Sharma, Shruti, Sanjiv Kumar, Saurabh Aggarwal, et al. "LPS Decreases Dimethylarginine Dimethylaminohydrolase (DDAH) Activity Through The Activation Of Pp60Src." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6476.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Bakr, Adel G. M., Natascha Sommer, Hossein Ghofrani, et al. "Effects Of Dimethylarginine Dimethylaminohydrolase 1 (DDAH-1) In Acute And Sustained Hypoxia Induced Pulmonary Vasoconstriction." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5497.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Lota, Harpreet K., та James M. Leiper. "Role of the nitric oxide-asymmetric dimethylarginine-dimethylarginine dimethylaminohydrolase (NO-ADMA-DDAH) axis in TGF-β mediated epithelial-mesenchymal transition". У Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa3049.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Bachmann, A., J. Singh, Y. Lee, M. Sturek, T. Karn, and N. Sänger. "Polyzystisches Ovarsyndrom (PCOS) und kardiovaskuläres Risiko: Unterschiede in der Aktivität von Dimethylarginin Dimethylaminohydrolase 1 (DDAH 1) in der Leber von Ossabaw Miniaturschweinen." In 62. Kongress der Deutschen Gesellschaft für Gynäkologie und Geburtshilfe – DGGG'18. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1671619.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Lota, HK, CJ Stock, EA Renzoni, AU Wells, and JM Leiper. "S141 A novel dimethylarginine dimethylaminohydrolase 1 (DDAH1) genetic variant associated with lower asymmetric dimethylarginine (ADMA) levels predicts accelerated lung function decline and mortality in idiopathic pulmonary fibrosis." In British Thoracic Society Winter Meeting 2018, QEII Centre, Broad Sanctuary, Westminster, London SW1P 3EE, 5 to 7 December 2018, Programme and Abstracts. BMJ Publishing Group Ltd and British Thoracic Society, 2018. http://dx.doi.org/10.1136/thorax-2018-212555.147.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'DDAH2' for particular source types:
Journal articles Dissertations / Theses
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography