Relevant bibliographies by topics / HTREK1

Academic literature on the topic 'HTREK1'

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Published: 6 September 2023

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Journal articles on the topic "HTREK1"

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Miller, Paula, Chris Peers, and Paul J. Kemp. "Polymodal regulation of hTREK1 by pH, arachidonic acid, and hypoxia: physiological impact in acidosis and alkalosis." American Journal of Physiology-Cell Physiology 286, no. 2 (February 2004): C272—C282. http://dx.doi.org/10.1152/ajpcell.00334.2003.

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Expression of the human tandem P domain K+ channel, hTREK1, is limited almost exclusively to the central nervous system, where ambient Po2 can be as low as 20 Torr. We have previously shown that this level of hypoxia evokes a maximal inhibitory influence on recombinant hTREK1 and occludes the activation by arachidonic acid; this has cast doubt on the idea that TREK1 activation during brain ischemia could facilitate neuroprotection via hyperpolarizing neurons in which it is expressed. Using both whole cell and cell-attached patch-clamp configurations, we now show that the action of another potent TREK activator and ischemia-related event, intracellular acidification, is similarly without effect during compromised O2 availability. This occlusion is observed in either recording condition, and even the concerted actions of both arachidonic acid and intracellular acidosis are unable to activate hTREK1 during hypoxia. Conversely, intracellular alkalinization is a potent channel inhibitor, and hypoxia does not reverse this inhibition. However, increases in intracellular pH are unable to occlude either arachidonic acid activation or hypoxic inhibition. These data highlight two important points. First, during hypoxia, modulation of hTREK1 cannot be accomplished by parameters known to be perturbed in brain ischemia (increased extracellular fatty acids and intracellular acidification). Second, the mechanism of regulation by intracellular alkalinization is distinct from the overlapping structural requirements known to exist for regulation by arachidonic acid, membrane distortion, and acidosis. Thus it seems likely that hTREK1 regulation in the brain will be physiologically more relevant during alkalosis than during ischemia or acidosis.
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Miller, P., P. J. Kemp, and C. Peers. "Structural requirements for O2 sensing by the human tandem-P domain channel, hTREK1." Biochemical and Biophysical Research Communications 331, no. 4 (June 2005): 1253–56. http://dx.doi.org/10.1016/j.bbrc.2005.04.042.

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Metri, Vishal, Swagata Ghatak, Soumyendu Raha, and S. K. Sikdar. "Patch clamp data driven stochastic modeling and simulation of hTREK1 potassium ion channel gating." Chemical Physics 516 (January 2019): 182–90. http://dx.doi.org/10.1016/j.chemphys.2018.07.030.

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El Hachmane, Mickael-F., Kathryn A. Rees, Emma L. Veale, Vadim V. Sumbayev, and Alistair Mathie. "Enhancement of TWIK-related Acid-sensitive Potassium Channel 3 (TASK3) Two-pore Domain Potassium Channel Activity by Tumor Necrosis Factor α." Journal of Biological Chemistry 289, no. 3 (December 4, 2013): 1388–401. http://dx.doi.org/10.1074/jbc.m113.500033.

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TASK3 two-pore domain potassium (K2P) channels are responsible for native leak K channels in many cell types which regulate cell resting membrane potential and excitability. In addition, TASK3 channels contribute to the regulation of cellular potassium homeostasis. Because TASK3 channels are important for cell viability, having putative roles in both neuronal apoptosis and oncogenesis, we sought to determine their behavior under inflammatory conditions by investigating the effect of TNFα on TASK3 channel current. TASK3 channels were expressed in tsA-201 cells, and the current through them was measured using whole cell voltage clamp recordings. We show that THP-1 human myeloid leukemia monocytes, co-cultured with hTASK3-transfected tsA-201 cells, can be activated by the specific Toll-like receptor 7/8 activator, R848, to release TNFα that subsequently enhances hTASK3 current. Both hTASK3 and mTASK3 channel activity is increased by incubation with recombinant TNFα (10 ng/ml for 2–15 h), but other K2P channels (hTASK1, hTASK2, hTREK1, and hTRESK) are unaffected. This enhancement by TNFα is not due to alterations in levels of channel expression at the membrane but rather to an alteration in channel gating. The enhancement by TNFα can be blocked by extracellular acidification but persists for mutated TASK3 (H98A) channels that are no longer acid-sensitive even in an acidic extracellular environment. TNFα action on TASK3 channels is mediated through the intracellular C terminus of the channel. Furthermore, it occurs through the ASK1 pathway and is JNK- and p38-dependent. In combination, TNFα activation and TASK3 channel activity can promote cellular apoptosis.
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Nayak, Tapan Kumar, Saswati Dana, Soumyendu Raha, and Sujit K. Sikdar. "Activator-induced dynamic disorder and molecular memory in human two-pore domain hTREK1 K+ channel." Journal of Chemical Biology 4, no. 2 (February 1, 2011): 69–84. http://dx.doi.org/10.1007/s12154-010-0053-3.

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Stueber, Thomas, Mirjam J. Eberhardt, Christoph Hadamitzky, Annette Jangra, Stefan Schenk, Felicia Dick, Carsten Stoetzer, et al. "Quaternary Lidocaine Derivative QX-314 Activates and Permeates Human TRPV1 and TRPA1 to Produce Inhibition of Sodium Channels and Cytotoxicity." Anesthesiology 124, no. 5 (May 1, 2016): 1153–65. http://dx.doi.org/10.1097/aln.0000000000001050.

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Abstract Background The relatively membrane-impermeable lidocaine derivative QX-314 has been reported to permeate the ion channels transient receptor potential vanilloid 1 (TRPV1) and transient receptor potential cation channel, subfamily A, member 1 (TRPA1) to induce a selective inhibition of sensory neurons. This approach is effective in rodents, but it also seems to be associated with neurotoxicity. The authors examined whether the human isoforms of TRPV1 and TRPA1 allow intracellular entry of QX-314 to mediate sodium channel inhibition and cytotoxicity. Methods Human embryonic kidney 293 (HEK-293) cells expressing wild-type or mutant human (h) TRPV1 or TRPA1 constructs as well as the sodium channel Nav1.7 were investigated by means of patch clamp and ratiometric calcium imaging. Cytotoxicity was examined by flow cytometry. Results Activation of hTRPA1 by carvacrol and hTRPV1 by capsaicin produced a QX-314–independent reduction of sodium current amplitudes. However, permeation of QX-314 through hTRPV1 or hTRPA1 was evident by a concentration-dependent, use-dependent inhibition of Nav1.7 activated at 10 Hz. Five and 30 mM QX-314 activated hTRPV1 via mechanisms involving the intracellular vanilloid-binding domain and hTRPA1 via unknown mechanisms independent of intracellular cysteins. Expression of hTRPV1, but not hTRPA1, was associated with a QX-314–induced cytotoxicity (viable cells 48 ± 5% after 30 mM QX-314) that was ameliorated by the TRPV1 antagonist 4-(3-chloro-2-pyridinyl)-N-[4-(1,1-dimethylethyl)phenyl]-1-piperazinecarboxamide (viable cells 81 ± 5%). Conclusions The study data demonstrate that QX-314 directly activates and permeates the human isoforms of TRPV1 and TRPA1 to induce inhibition of sodium channels, but also a TRPV1-dependent cytotoxicity. These results warrant further validation of this approach in more intact preparations and may be valuable for the development of this concept into clinical practice.
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Gil, V., D. Gallego, H. Moha Ou Maati, R. Peyronnet, M. Martínez-Cutillas, C. Heurteaux, M. Borsotto, and M. Jiménez. "Relative contribution of SKCa and TREK1 channels in purinergic and nitrergic neuromuscular transmission in the rat colon." American Journal of Physiology-Gastrointestinal and Liver Physiology 303, no. 3 (August 1, 2012): G412—G423. http://dx.doi.org/10.1152/ajpgi.00040.2012.

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Purinergic and nitrergic neurotransmission predominantly mediate inhibitory neuromuscular transmission in the rat colon. We studied the sensitivity of both purinergic and nitrergic pathways to spadin, a TWIK-related potassium channel 1 (TREK1) inhibitor, apamin, a small-conductance calcium-activated potassium channel blocker and 1H-[1,2,4]oxadiazolo[4,3-α]quinoxalin-1-one (ODQ), a specific inhibitor of soluble guanylate cyclase. TREK1 expression was detected by RT-PCR in the rat colon. Patch-clamp experiments were performed on cells expressing hTREK1 channels. Spadin (1 μM) reduced currents 1) in basal conditions 2) activated by stretch, and 3) with arachidonic acid (AA; 10 μM). l-Methionine (1 mM) or l-cysteine (1 mM) did not modify currents activated by AA. Microelectrode and muscle bath studies were performed on rat colon samples. l-Methionine (2 mM), apamin (1 μM), ODQ (10 μM), and Nω-nitro-l-arginine (l-NNA; 1 mM) depolarized smooth muscle cells and increased motility. These effects were not observed with spadin (1 μM). Purinergic and nitrergic inhibitory junction potentials (IJP) were studied by incubating the tissue with l-NNA (1 mM) or MRS2500 (1 μM). Both purinergic and nitrergic IJP were unaffected by spadin. Apamin reduced both IJP with a different potency and maximal effect for each. ODQ concentration dependently abolished nitrergic IJP without affecting purinergic IJP. Similar effects were observed in hyperpolarizations induced by sodium nitroprusside (1 μM) and nitrergic relaxations induced by electrical stimulation. We propose a pharmacological approach to characterize the pathways and function of purinergic and nitrergic neurotransmission. Nitrergic neurotransmission, which is mediated by cyclic guanosine monophosphate, is insensitive to spadin, an effective TREK1 channel inhibitor. Both purinergic and nitrergic neurotransmission are inhibited by apamin but with different relative sensitivity.
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Wiedmann, Felix, Daniel Schlund, Francisco Faustino, Manuel Kraft, Antonius Ratte, Dierk Thomas, Hugo A. Katus, and Constanze Schmidt. "N-Glycosylation of TREK-1/hK2P2.1 Two-Pore-Domain Potassium (K2P) Channels." International Journal of Molecular Sciences 20, no. 20 (October 20, 2019): 5193. http://dx.doi.org/10.3390/ijms20205193.

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Mechanosensitive hTREK-1 two-pore-domain potassium (hK2P2.1) channels give rise to background currents that control cellular excitability. Recently, TREK-1 currents have been linked to the regulation of cardiac rhythm as well as to hypertrophy and fibrosis. Even though the pharmacological and biophysical characteristics of hTREK-1 channels have been widely studied, relatively little is known about their posttranslational modifications. This study aimed to evaluate whether hTREK-1 channels are N-glycosylated and whether glycosylation may affect channel functionality. Following pharmacological inhibition of N-glycosylation, enzymatic digestion or mutagenesis, immunoblots of Xenopus laevis oocytes and HEK-293T cell lysates were used to assess electrophoretic mobility. Two-electrode voltage clamp measurements were employed to study channel function. TREK-1 channel subunits undergo N-glycosylation at asparagine residues 110 and 134. The presence of sugar moieties at these two sites increases channel function. Detection of glycosylation-deficient mutant channels in surface fractions and recordings of macroscopic potassium currents mediated by these subunits demonstrated that nonglycosylated hTREK-1 channel subunits are able to reach the cell surface in general but with seemingly reduced efficiency compared to glycosylated subunits. These findings extend our understanding of the regulation of hTREK-1 currents by posttranslational modifications and provide novel insights into how altered ion channel glycosylation may promote arrhythmogenesis.
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Oates, David, Wendy Nice, Roy Taylor, and Wendy Hanson. "Porous ceramics for gas turbine applications." High Temperatures-High Pressures 27/28, no. 3 (1995): 339–45. http://dx.doi.org/10.1068/htrt01.

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Dozhdikov, Vitaly, and Vadim Petrov. "New automated apparatus for the measurement of spectral emissivity of nonconducting materials by high-speed spectrometer." High Temperatures-High Pressures 27/28, no. 4 (1995): 403–10. http://dx.doi.org/10.1068/htrt41.

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Dissertations / Theses on the topic "HTREK1"

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Miller, Paula. "Oxygen sensing by hTREK1, a twin-pore-domain potassium channel." Thesis, University of Leeds, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.403031.

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FANTONE, SONIA. "Role of HtrA1 in pregnancy: a possible early marker of Preeclampsia." Doctoral thesis, Università Politecnica delle Marche, 2021. http://hdl.handle.net/11566/289654.

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L’ High temperature requirement A 1 (HtrA1), un membro della famiglia HtrA, è una proteina di secrezione multidominio con attività serin-proteasica. Alcuni studi suggeriscono che questa proteina sia coinvolta nello sviluppo fisiologico di alcuni organi, compresa la placenta. Inoltre, è stata dimostrata un'alterazione dell'espressione di HtrA1 in vari carcinomi e in alcune malattie placentari come la preeclampsia (PE). La PE è una sindrome gestazionale che colpisce il 3-5% della gravidanza nel mondo, caratterizzata dalla nuova insorgenza di ipertensione e proteinuria materna. Sebbene i sintomi della PE compaiano dopo la 20° settimana di gestazione, la patologia inizia a svilupparsi prima di questo periodo. Una corretta identificazione prima delle 12 settimane di gestazione delle donne che svilupperanno la PE durante la gravidanza, potrebbe consentire di trattare le gestanti ad alto rischio di PE prima della comparsa dei sintomi al fine di prevenire danni alla placenta e di conseguenza al feto. È interessante notare che l'espressione dell’HtrA1 era alterata sia nel tessuto placentare che nel plasma materno delle gravidanze complicate da PE. Pertanto, l’HtrA1 potrebbe essere una molecola chiave nello sviluppo di questa malattia, nonché un marker utile per la sua diagnosi e cura. Lo scopo di questo studio è valutare se l’HtrA1 possa essere considerato un utile marker precoce dell'insorgenza di PE e come l'espressione dell’HtrA1 possa essere modificata attraverso la somministrazione di sostanze di uso comune e innovative per il trattamento di PE. L'identificazione di un marker predittivo di PE e di possibili nuovi approcci terapeutici per la gestione della PE è attualmente una delle questioni ginecologiche più rilevanti, al fine di ridurre il rischio di mortalità e morbilità materna e fetale.
The High temperature requirement A 1 (HtrA1), a member of the HtrA family, is a multidomain secretory protein with serine-protease activity. Some studies suggest that this protein is involved in physiological development of some organs including the placenta. Furthermore, it has been proved an alteration in HtrA1 expression in various carcinomas and in some placental disease such as preeclampsia (PE). PE is a gestational syndrome that affect the 3-5% of the pregnancy worldwide, characterized by new onset of maternal hypertension and proteinuria. Although PE symptoms appear after 20th week of gestation, the pathology begins to develop before this period. A correct identification of pregnant woman that will develop PE, before 12 weeks of gestation, makes it possible to manage women at high risk of PE before the appearance of symptoms in order to prevent damage to the placenta and consequently to the fetus. It is interesting to note that HtrA1 expression was altered in both placental tissue and maternal plasma of pregnancies complicated by PE. Therefore, HtrA1 could be considered a key molecule in the development of this disease. The aim of this study is to evaluate: i) whether the HtrA1 protein could be considered a useful early marker of PE onset and ii) how common and innovative compounds for treatment of PE modify the HtrA1 expression. In conclusion, the identification of a predictive markers of PE and possible new therapeutic approaches for the management of PE is currently one of the relevant gynecological issues in order to reduce the risk of maternal and fetal mortality and morbidity.
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Scharrer, Eva. "Consequences of HtrA1 deficiency on TGF-Beta signaling." Diss., Ludwig-Maximilians-Universität München, 2015. http://nbn-resolving.de/urn:nbn:de:bvb:19-185742.

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Verdura, Edgard. "Familial Cerebral Small Vessel Diseases of unknown etiology : a high throughput approach towards a better understanding of pathophysiological mechanisms." Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCC264.

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Les maladies des petites artères cérébrales sont un groupe hétérogène de maladies qui affectent les petites artères, artérioles, veines et/ou capillaires du cerveau. La plupart des patients sont des cas sporadiques, mais plusieurs formes héréditaires ont été identifiées.Toutefois, 15 % seulement des patients atteints d’une cSVD familiale sont porteurs d’une mutation dans l’un de ces gènes, suggérant l’implication d’autres gènes. Dans cette thèse, nous avons montré que des mutations hétérozygotes du gène HTRA1 étaient responsables d’environ 5 % des cSVD familiales. L’analyse fonctionnelle de ces mutations a montré un effet perte de fonction. L’âge de début chez les sujets hétérozygotes était beaucoup plus tardif que chez les patients CARASIL, où les deux allèles d’HTRA1 sont mutés. Ensuite, nous avons identifié 2 familles (incluant la famille rapportée sous l’acronyme PADMAL / Pontine Autosomal Dominant Microangiopathy and Leukoencephalopathy) portant deux mutations distinctes dans un site d’accrochage du microRNA miR-29, dans la partie 3’UTR du gène COL4A1.Quatre autres patients index porteurs du même type de mutations ont été identifiés dans notre cohorte de cas cSVD. L’analyse fonctionnelle de ces mutations a mis en évidence une up-régulation de l’expression du gène COL4A1. Le phénotype observé était très stéréotypé, caractérisé par la survenue d’infarctus pontiques dans la 3ème décade. L’identification des bases moléculaires de ces deux nouvelles formes de cSVD héréditaire a des applications diagnostiques immédiates. Elle renforce par ailleurs l’hypothèse du rôle essentiel d’une altération du matrisome dans les mécanismes physiopathologiques des cSVD
Cerebral small vessel diseases (cSVD) are a heterogeneous group of disorders affecting small arteries, arterioles, veins, and/or capillaries of the brain. In most cases cSVD are sporadic, but several hereditary monogenic forms have been identified. Nevertheless, only 15% of familial cSVD patients sent for genetic screening are carriers of mutations in one of these genes, suggesting the implication of other genes. In this thesis work, we showed that heterozygous mutations in HTRA1 are found in 5% of familial cSVD cases. Functional analysis of these mutations showed that most of them behave as loss-of-function mutations. Disease onset was much later (>25 years) than in CARASIL patients, in which both2 HTRA1 alleles are mutated. Afterwards, we identified 2 informative families (including the original family reported to be affected by PADMAL / Pontine Autosomal Dominant Microangiopathy and Leukoencephalopathy) harboring two different mutations in the binding site of miR-29 microRNA within the 3’UTR of COL4A1 gene. Four other index patients carrying the same type of mutations were identified in our patient cohort. Functional analysis of these mutations showed an up-regulation of COL4A1 gene expression. The observed phenotype was highly stereotyped in all patients, characterized by pontine infarcts appearing in the 3rd decade. Identification of the molecular defects underlying these two novel hereditary cSVD forms provides tools to improve the molecular diagnosis of cSVD. Besides, it reinforces the hypothesis of an essential role of matrisome alteration in cSVD pathophysiological mechanisms
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Yamawaki, Satoko. "HtrA1 Is Specifically Up-Regulated in Active Keloid Lesions and Stimulates Keloid Development." Kyoto University, 2019. http://hdl.handle.net/2433/245295.

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Stuqui, Bruna [UNESP]. "Caracterização funcional de HTRA1 em linhagens celulares HPV positiva e HPV negativa." Universidade Estadual Paulista (UNESP), 2014. http://hdl.handle.net/11449/111013.

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
O Papilomavirus humano (HPV) é um dos vírus mais prevalentes entre as infecções sexualmente transmissíveis e está associado com doenças malignas. Os HPVs de alto risco possuem proteínas, denominadas de E6 e E7, caracterizadas como oncoproteínas devido aos seus papéis na transformação celular e na inativação de supressores de tumor. Um dos mecanismos usados na transformação celular pela proteína E6 do HPV de alto risco é a interação do seu domínio carboxi-terminal, PDZ, com domínios PDZs presentes em algumas proteínas celulares, destinando-as à degradação. Uma proteína que está associada com várias condições patológicas e tem domínio PDZ é a protease HtrA1. Esta proteína é pouco expressa em alguns cânceres, sugerindo um papel supressor de tumor. O objetivo deste estudo foi avaliar o efeito da superexpressão de HTRA1 em linhagem celular HPV16 positiva (HF698) e HPV negativa (C33). As linhagens celulares foram transfectadas com vetor contendo a ORF de HTRA1 ou vetor vazio. A superexpressão do mRNA e proteína foi confirmada por qPCR e imuno-histoquímica, respectivamente. As linhagens celulares transfectadas foram submetidas a ensaio de formação de colônia, de viabilidade celular, de apoptose e ciclo celular. As células C33 superexpressando HtrA1 formaram significantemente menos colônias e apresentaram redução de viabilidade celular comparadas as células sem expressão de HtrA1. Diferentemente, na linhagem HPV positiva ocorreu aumento no número de colônias nas células superexpressando HtrA1 e não houve diferença no ensaio de viabilidade celular. Esses resultados sugerem que os diferentes padrões observados nas duas linhagens celulares são decorrentes da presença do HPV na HF698 e da ausência na C33. A fim de confirmar se o aumento do número de colônias nas células HF698 superexpressando HtrA1 é decorrente da interação dessa proteína com E6, foi produzida linhagem estável de C33 com ...
The Human Papillomavirus (HPV) is one of the most prevalent virus among sexually transmitted infections and it is associated with some malignancies. High risk HPVs contain proteins, E6 and E7, characterized by oncoproteins due to their roles in cellular transformation and suppressor tumor inactivation. One of the mechanisms used in cell transformation by E6 protein from high-risk HPVs is the interaction of its carboxy-terminal domain, known as PDZ, with PDZs domains present in some cellular proteins, triggering them to degradation. A protein that is associated with various pathological conditions and has PDZ domain is the protease HtrA1. This protein is poorly expressed in some cancers, suggesting its tumor suppressor role. The aim of this study was to evaluate the effect of the HtrA1 overexpression in HPV 16 positive (HF698) and HPV negative (C33) cell lines. The cell lines were transfected with vector containing the HTRA1 ORF or empty vector. The mRNA and protein overexpression were confirmed by qPCR and immunohistochemical, respectively. The cell lines transfected were subjected to cell proliferation, viability, apoptosis and cell cycle assays. C33 cells expressing HtrA1 presented significantly fewer colonies and showed reduced viability than cells without HtrA1 expression. On the other hand, in HPV-positive cell line there was an increase in the number of colonies in cells expressing HtrA1 and there was no difference in the cell viability assay. These results suggest that the different patterns observed between the two cell lines studied may be due to the HPV presence in HF698 and its absence in C33 cells. To confirm if the increase in the number of colonies in HPV positive cells (HF698) overexpressing HtrA1 arises from the interaction of this protein with E6, stable lines of C33 containing gene E6 were produced and subsequently performed cell proliferation assay. C33 cells overexpressing E6 and HTRA1 showed an increased number of ...
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Stuqui, Bruna. "Caracterização funcional de HTRA1 em linhagens celulares HPV positiva e HPV negativa /." São José do Rio Preto, 2014. http://hdl.handle.net/11449/111013.

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Orientador: Marilia de Freitas Calmon
Coorientador: Paula Rahal
Banca: Carolina Colombelli Pacca
Banca: Sebastião Roberto Taboga
Resumo: O Papilomavirus humano (HPV) é um dos vírus mais prevalentes entre as infecções sexualmente transmissíveis e está associado com doenças malignas. Os HPVs de alto risco possuem proteínas, denominadas de E6 e E7, caracterizadas como oncoproteínas devido aos seus papéis na transformação celular e na inativação de supressores de tumor. Um dos mecanismos usados na transformação celular pela proteína E6 do HPV de alto risco é a interação do seu domínio carboxi-terminal, PDZ, com domínios PDZs presentes em algumas proteínas celulares, destinando-as à degradação. Uma proteína que está associada com várias condições patológicas e tem domínio PDZ é a protease HtrA1. Esta proteína é pouco expressa em alguns cânceres, sugerindo um papel supressor de tumor. O objetivo deste estudo foi avaliar o efeito da superexpressão de HTRA1 em linhagem celular HPV16 positiva (HF698) e HPV negativa (C33). As linhagens celulares foram transfectadas com vetor contendo a ORF de HTRA1 ou vetor vazio. A superexpressão do mRNA e proteína foi confirmada por qPCR e imuno-histoquímica, respectivamente. As linhagens celulares transfectadas foram submetidas a ensaio de formação de colônia, de viabilidade celular, de apoptose e ciclo celular. As células C33 superexpressando HtrA1 formaram significantemente menos colônias e apresentaram redução de viabilidade celular comparadas as células sem expressão de HtrA1. Diferentemente, na linhagem HPV positiva ocorreu aumento no número de colônias nas células superexpressando HtrA1 e não houve diferença no ensaio de viabilidade celular. Esses resultados sugerem que os diferentes padrões observados nas duas linhagens celulares são decorrentes da presença do HPV na HF698 e da ausência na C33. A fim de confirmar se o aumento do número de colônias nas células HF698 superexpressando HtrA1 é decorrente da interação dessa proteína com E6, foi produzida linhagem estável de C33 com ...
Abstract: The Human Papillomavirus (HPV) is one of the most prevalent virus among sexually transmitted infections and it is associated with some malignancies. High risk HPVs contain proteins, E6 and E7, characterized by oncoproteins due to their roles in cellular transformation and suppressor tumor inactivation. One of the mechanisms used in cell transformation by E6 protein from high-risk HPVs is the interaction of its carboxy-terminal domain, known as PDZ, with PDZs domains present in some cellular proteins, triggering them to degradation. A protein that is associated with various pathological conditions and has PDZ domain is the protease HtrA1. This protein is poorly expressed in some cancers, suggesting its tumor suppressor role. The aim of this study was to evaluate the effect of the HtrA1 overexpression in HPV 16 positive (HF698) and HPV negative (C33) cell lines. The cell lines were transfected with vector containing the HTRA1 ORF or empty vector. The mRNA and protein overexpression were confirmed by qPCR and immunohistochemical, respectively. The cell lines transfected were subjected to cell proliferation, viability, apoptosis and cell cycle assays. C33 cells expressing HtrA1 presented significantly fewer colonies and showed reduced viability than cells without HtrA1 expression. On the other hand, in HPV-positive cell line there was an increase in the number of colonies in cells expressing HtrA1 and there was no difference in the cell viability assay. These results suggest that the different patterns observed between the two cell lines studied may be due to the HPV presence in HF698 and its absence in C33 cells. To confirm if the increase in the number of colonies in HPV positive cells (HF698) overexpressing HtrA1 arises from the interaction of this protein with E6, stable lines of C33 containing gene E6 were produced and subsequently performed cell proliferation assay. C33 cells overexpressing E6 and HTRA1 showed an increased number of ...
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Tahmaseb, Kambiz. "Biochemical Characterization of hTRF1 and hTEP1, Two Proteins Involved in Telomere Maintenance." Wright State University / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=wright1182306717.

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Stanton, Chloe May. "Investigating the genetic and molecular basis of age-related macular degeneration." Thesis, University of Edinburgh, 2012. http://hdl.handle.net/1842/9608.

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Age-related macular degeneration (AMD) is the leading cause of blindness worldwide, affecting an estimated 50 million individuals aged over 65 years. Environmental and genetic risk-factors contribute to the development of AMD. An AMD-risk locus on chromosome 10q26 spans two genes, ARMS2 and HTRA1, and controversy exists as to which variants are responsible for increased risk of disease. Recent work suggests that HTRA1 expression levels are significantly increased in carriers of the risk haplotype associated with AMD. However, relatively little is known about the interactions, substrate specificity and roles in disease played by this secreted serine protease. This thesis aims to elucidate the potential role played by HTRA1 in AMD pathogenesis. A combination of tandem affinity purification (TAP) and yeast two-hybrid techniques was used to identify interacting partners of HTRA1. A number of proteins, with diverse roles in the alternative complement pathway, cell signaling, cell-matrix interactions, inflammation, angiogenesis and fibrosis, were identified. These are attractive candidates for further study as such processes are disturbed in AMD, implicating HTRA1 and its binding partners in disease development. One interacting partner, Complement Factor D (CFD), is a key activator in the alternative complement pathway. CFD, a 24 kDa serine protease, is expressed as an inactive zymogen, from which a signal peptide and activation peptide are cleaved before release of the mature, active protein into the circulation. In vitro studies show that CFD interacts with, and can be a substrate for, HTRA1. The interacting domain between the two proteins is localised to a region of 30 amino acids at the N-terminal end of proCFD. The 5 amino acid pro-peptide of CFD appears to be both necessary and sufficient for proteolysis of CFD by HTRA1. Investigation of the functional relevance of the interaction between HTRA1 and CFD shows that proCFD is cleaved by HTRA1, whilst mature CFD is not subjected to proteolysis. HTRA1-mediated cleavage of CFD forms an active protease, leading to activation of factor B in the alternative complement pathway in in vitro assays. Furthermore, a normal complement response is restored to CFD-depleted serum by addition of proCFD activated by HTRA1. Thus, an HTRA1- mediated increase in alternative complement pathway activity may explain a proportion of the AMD-risk attributed to the chr10q26 locus. Genetic and protein-based approaches were used to study the potential role of CFD in AMD pathogenesis, independent of an interaction with HTRA1. An intronic SNP, rs3826945, was significantly associated with increased risk of AMD in two British case-control cohorts, and in a combined meta-analysis with 4 additional cohorts from North America and Europe (p-value = 0.032, Odds Ratio = 1.112 in 4765 cases and 2693 controls). Assessment of copy number variation and sequencing of CFD did not identify any functional variants which may explain the association with disease. However, plasma levels of CFD were measured by ELISA in 751 AMD cases and 474 controls, and were found to be significantly elevated in AMD cases compared to controls (p-value = 0.00025). This further implicates complement activation in AMD pathogenesis, and makes CFD an attractive candidate for therapeutic intervention. An alteration in the level of activated CFD, possibly mediated via an interaction with HTRA1, either at the systemic or local tissue level, may play a role in disease development and progression.
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Scharrer, Eva [Verfasser], and Christian [Akademischer Betreuer] Wahl-Schott. "Consequences of HtrA1 deficiency on TGF-Beta signaling / Eva Scharrer. Betreuer: Christian Wahl-Schott." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2015. http://d-nb.info/1075457033/34.

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Books on the topic "HTREK1"

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Weygandt, Jerry J. Accounting Principles with CD 6e Volume 1 and Peac Htree Complete Accounting Set. John Wiley & Sons Inc, 2001.

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Book chapters on the topic "HTREK1"

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Akhtar-Schaefer, Isha, Raphael Reuten, Manuel Koch, Markus Pietsch, and Thomas Langmann. "AMD-Associated HTRA1 Variants Do Not Influence TGF-β Signaling in Microglia." In Retinal Degenerative Diseases, 3–7. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-27378-1_1.

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Kortvely, Elod, and Marius Ueffing. "Gene Structure of the 10q26 Locus: A Clue to Cracking the ARMS2/HTRA1 Riddle?" In Retinal Degenerative Diseases, 23–29. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-17121-0_4.

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Chien, Jeremy, and Viji Shridhar. "HtrA1 Peptidase." In Handbook of Proteolytic Enzymes, 2577–84. Elsevier, 2013. http://dx.doi.org/10.1016/b978-0-12-382219-2.00571-8.

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Conference papers on the topic "HTREK1"

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"NGRI1, PIP4K2A, and HTR2K contain possible genetics." In Bioinformatics of Genome Regulation and Structure/ Systems Biology. institute of cytology and genetics siberian branch of the russian academy of science, Novosibirsk State University, 2020. http://dx.doi.org/10.18699/bgrs/sb-2020-408.

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Mandal, Ayan, Sunil P. Khatri, and Rabi N. Mahapatra. "A source-synchronous Htree-based network-on-chip." In the 23rd ACM international conference. New York, New York, USA: ACM Press, 2013. http://dx.doi.org/10.1145/2483028.2483083.

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He, Xiaoping, Ashwani Khurana, Jacie L. Maguire, Jeremy Chien, and Viji Shridhar. "Abstract 1531: HtrA1 sensitizes ovarian cancer cells to cisplatin-induced cytotoxicity by targeting XIAP for degradation." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-1531.

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Cooley, Megan, Jeremy Chien, Anirban Mitra, Alfonso Baldi, Andras Czirok, and Edina Kosa. "Abstract 2385: Characterization of ECM remodeling in disseminated ovarian cancer as a result of loss of HtrA1 and deregulated TGFB signaling." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-2385.

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Ohta, Tsuyoshi, Ashwani Khurana, Jacie Maguire, Xiaoping He, Jeremy Chien, Keith Bible, and Viji Shridhar. "Abstract 4015: Flavopiridol-induced upregulation of HtrA1 is associated with suppression of its negative transcriptional regulator WT-1 and with enhanced chemosensitivity." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-4015.

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Cooley, Megan K., and Jeremy Chien. "Abstract POSTER-BIOL-1310: Regulation of tumor dormancy by extracellular matrix remodeling as a result of increased TGF-beta signaling and loss of HtrA1 in ovarian cancer." In Abstracts: 10th Biennial Ovarian Cancer Research Symposium; September 8-9, 2014; Seattle, WA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1557-3265.ovcasymp14-poster-biol-1310.

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Clark, T., J. F. Bobo, F. Mancoff, Kyusik Sin, Shan Wang, B. Clemens, and R. Sinclair. "HTREM study of Al/sub 2/O/sub 3/ barriers in Co/sub 81/Pt/sub 19//Co/Al-Al/sub 2/O/sub 3//Ni/sub 80/Fe/sub 20/ spin dependent tunneling junctions." In IEEE International Magnetics Conference. IEEE, 1999. http://dx.doi.org/10.1109/intmag.1999.837346.

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