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Добірка наукової літератури з теми "Adenosine pathway"

Автор: Grafiati
Опубліковано: 29 березня 2025

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Статті в журналах з теми "Adenosine pathway"

1

Ling, Chunyan, Liangcheng Shang, Xin Xie, Sudan Ye, Ningjing Wang, and Chun Chen. "AdoR-1 (Adenosine Receptor) Contributes to Protection against Paraquat-Induced Oxidative Stress in Caenorhabditis elegans." Oxidative Medicine and Cellular Longevity 2022 (December 22, 2022): 1–13. http://dx.doi.org/10.1155/2022/1759009.

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AdoR-1, the single adenosine receptor homolog in Caenorhabditis elegans, which belongs to the superfamily of G-protein coupled receptors (GPCRs), mediates most of the physiological effects of extracellular adenosine. Adenosine has been proved to improve the survival rate of C. elegans in oxidative stress conditions. However, the potential mechanism of adenosine’s protective effect against oxidative stress via AdoR-1 has not been studied. In this study, C. elegans were divided into three groups: two groups with paraquat treatment, one in the presence and one in the absence of adenosine, and an untreated control group. Results indicate that many differentially expressed genes were found to be enriched significantly in neural-related signaling pathways among transcriptome data of three groups. Further gene network analysis showed that some important genes well known to be involved in promoting the acetylcholine release pathway, such as dop-1, egl-30, and unc-13, and those involved in promoting the neuropeptide release pathway, such as kin-1, were upregulated by paraquat induction but downregulated after adenosine treatment. Meanwhile, a completely opposite trend was observed for the goa-1 gene that inhibits the acetylcholine-release and neuropeptide-release pathway. Additionally, some biochemical assays including SOD, GSSG, GSH, and AChE were measured to identify the potential protection of adenosine against oxidative stress between wild-type strain N2 and ador-1 gene knockout strain EG6890. Conclusively, our study revealed series of adenosine receptor-mediated genes in C. elegans that might act as regulators of paraquat-induced oxidative stress and may indicate adenosine’s promising protective effects.
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2

Jackson, Edwin K., and Raghvendra K. Dubey. "Role of the extracellular cAMP-adenosine pathway in renal physiology." American Journal of Physiology-Renal Physiology 281, no. 4 (October 1, 2001): F597—F612. http://dx.doi.org/10.1152/ajprenal.2001.281.4.f597.

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Adenosine exerts physiologically significant receptor-mediated effects on renal function. For example, adenosine participates in the regulation of preglomerular and postglomerular vascular resistances, glomerular filtration rate, renin release, epithelial transport, intrarenal inflammation, and growth of mesangial and vascular smooth muscle cells. It is important, therefore, to understand the mechanisms that generate extracellular adenosine within the kidney. In addition to three “classic” pathways of adenosine biosynthesis, contemporary studies are revealing a novel mechanism for renal adenosine production termed the “extracellular cAMP-adenosine pathway.” The extracellular cAMP-adenosine pathway is defined as the egress of cAMP from cells during activation of adenylyl cyclase, followed by the extracellular conversion of cAMP to adenosine by the serial actions of ecto-phosphodiesterase and ecto-5′-nucleotidase. This mechanism of extracellular adenosine production may provide hormonal control of adenosine levels in the cell-surface biophase in which adenosine receptors reside. Tight coupling of the site of adenosine production to the site of adenosine receptors would permit a low-capacity mechanism of adenosine biosynthesis to have a large impact on adenosine receptor activation. The purposes of this review are to summarize the physiological roles of adenosine in the kidney; to describe the classic pathways of renal adenosine biosynthesis; to review the evidence for the existence of the extracellular cAMP-adenosine pathway; and to describe possible physiological roles of the extracellular cAMP-adenosine pathway, with particular emphasis on the kidney.
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3

Jackson, Edwin K., Jin Ren, Dongmei Cheng, and Zaichuan Mi. "Extracellular cAMP-adenosine pathways in the mouse kidney." American Journal of Physiology-Renal Physiology 301, no. 3 (September 2011): F565—F573. http://dx.doi.org/10.1152/ajprenal.00094.2011.

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The renal extracellular 2′,3′-cAMP-adenosine and 3′,5′-cAMP-adenosine pathways (extracellular cAMPs→AMPs→adenosine) may contribute to renal adenosine production. Because mouse kidneys provide opportunities to investigate renal adenosine production in genetically modified kidneys, it is important to determine whether mouse kidneys express these cAMP-adenosine pathways. We administered (renal artery) 2′,3′-cAMP and 3′,5′-cAMP to isolated, perfused mouse kidneys and measured renal venous secretion rates of 2′,3′-cAMP, 3′,5′-cAMP, 2′-AMP, 3′-AMP, 5′-AMP, adenosine, and inosine. Arterial infusions of 2′,3′-cAMP increased ( P < 0.0001) the mean venous secretion of 2′-AMP (390-fold), 3′-AMP (497-fold), adenosine (18-fold), and inosine (adenosine metabolite; 7-fold), but they did not alter 5′-AMP secretion. Infusions of 3′,5′-cAMP did not affect venous secretion of 2′-AMP or 3′-AMP, but they increased ( P < 0.0001) secretion of 5′-AMP (5-fold), adenosine (17-fold), and inosine (6-fold). Energy depletion (metabolic inhibitors) increased the secretion of 2′,3′-cAMP (8-fold, P = 0.0081), 2′-AMP (4-fold, P = 0.0028), 3′-AMP (4-fold, P = 0.0270), 5′-AMP (3-fold, P = 0.0662), adenosine (2-fold, P = 0.0317), and inosine (7-fold, P = 0.0071), but it did not increase 3′,5′-cAMP secretion. The 2′,3′-cAMP-adenosine pathway was quantitatively similar in CD73 −/− vs. +/+ kidneys. However, 3′,5′-cAMP induced a 6.7-fold greater increase in 5′-AMP, an attenuated increase (61% reduction) in inosine and a similar increase in adenosine in CD73 −/− vs. CD73 +/+ kidneys. In mouse kidneys, 1) 2′,3′-cAMP and 3′,5′-cAMP are metabolized to their corresponding AMPs, which are subsequently metabolized to adenosine; 2) energy depletion activates the 2′,3′-cAMP-adenosine, but not the 3′,5′-cAMP-adenosine, pathway; and 3) although CD73 is involved in the 3′,5′-AMP-adenosine pathway, alternative pathways of 5′-AMP metabolism and reduced metabolism of adenosine to inosine compensate for life-long deficiency of CD73.
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4

Dorostkar, Parvin C., Macdonald Dick, Gerald A. Serwer, Sarah LeRoy, and Brian Armstrong. "Effect of adenosine on atrioventricular conduction in children and young patients with supraventricular tachycardia." Cardiology in the Young 6, no. 4 (October 1996): 308–14. http://dx.doi.org/10.1017/s1047951100003930.

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AbstractAdenosine, when given as an intravenous bolus, has been shown to produce atrioventricular nodal block in humans. To examine the effect of adenosine on conduction across both accessory pathways and the atrioventricular node in children, we reviewed our experience with adenosine administered during both atrial and ventricular pacing in 42 patients with atrioventricular resting tachycardia and in eight patients with atrioventricular nodal reentry tachycardia. Adenosine was administered as a mean bolus of 195 μg/kg/dose during both atrial and ventricular pacing, examining antegrade and retrograde conduction before and after radiofrequency ablation. In those patients with persistent or intermittent pre-excitation, anomalous ventricular activation was either unchanged (n=8) or increased (n=11). Retrograde conduction (either through the accessory pathway alone in three, or across both the accessory pathway and the atrioventricular node in 19) persisted in 92% of the 24 patients studied. Adenosine produced either first or third degree antegrade heart block in all patients studied without pre-excitation (those with either dual atrioventricular nodal pathways or concealed accessory pathways). Adenosine produced retrograde block in all of the eight patients with dual atrioventricular nodal pathways. In contrast, retrograde conduction persisted in 82% (14/17) of patients with concealed accessory pathways (p=0.001). When used to examine retrograde conduction, adenosine was a sensitive (82%) and highly specific (producing retrograde atrioventricular block in all patients with dual atrioventricular nodal pathways) predictor of tachycardia supported by a concealed accessory pathway. Adenosine yielded a sensitivity and specificity of 96% and a positive predictive value of 99.5% for the success of ablation of accessory pathways. These data indicate that the pattern of adenosine-induced changes in either antegrade or retrograde atrioventricular conduction, or conduction in both directions, in young patients with supraventricular tachycardia is related to the mechanism of the tachycardia. Adenosine, therefore, is a useful adjunct in the electrophysiologic evaluation of supraventricular tachycardia in children.
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5

LAPAGE, MARTIN J., MICHAEL J. WALSH, JOHN H. REED, and J. PHILIP SAUL. "Adenosine Mapping for Adenosine-Dependent Accessory Pathway Ablation." Pacing and Clinical Electrophysiology 37, no. 5 (December 20, 2013): 610–15. http://dx.doi.org/10.1111/pace.12324.

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6

Jackson, Edwin K. "The 2′,3′-cAMP-adenosine pathway." American Journal of Physiology-Renal Physiology 301, no. 6 (December 2011): F1160—F1167. http://dx.doi.org/10.1152/ajprenal.00450.2011.

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Анотація:
Our recent studies employing HPLC-tandem mass spectrometry to analyze venous perfusate from isolated, perfused kidneys demonstrate that intact kidneys produce and release into the extracellular compartment 2′,3′-cAMP, a positional isomer of the second messenger 3′,5′-cAMP. To our knowledge, this represents the first detection of 2′,3′-cAMP in any cell/tissue/organ/organism. Nuclear magnetic resonance experiments with isolated RNases and experiments in isolated, perfused kidneys suggest that 2′,3′-cAMP likely arises from RNase-mediated transphosphorylation of mRNA. Both in vitro and in vivo kidney experiments demonstrate that extracellular 2′,3′-cAMP is efficiently metabolized to 2′-AMP and 3′-AMP, both of which can be further metabolized to adenosine. This sequence of reactions is called the 2′,3′-cAMP-adenosine pathway (2′,3′-cAMP → 2′-AMP/3′-AMP → adenosine). Experiments in rat and mouse kidneys show that metabolic poisons increase extracellular levels of 2′,3′-cAMP, 2′-AMP, 3′-AMP, and adenosine; however, little is known regarding the pharmacology of 2′,3′-cAMP, 2′-AMP, and 3′-AMP. What is known is that 2′,3′-cAMP facilitates activation of mitochondrial permeability transition pores, a process that can lead to apoptosis and necrosis, and inhibits proliferation of vascular smooth muscle cells and glomerular mesangial cells. In summary, there is mounting evidence that at least some types of cellular injury, by triggering mRNA degradation, engage the 2′,3′-cAMP-adenosine pathway, and therefore this pathway should be added to the list of biochemical pathways that produce adenosine. Although speculative, it is possible that the 2′,3′-cAMP-adenosine pathway may protect against some forms of acute organ injury, for example acute kidney injury, by both removing an intracellular toxin (2′,3′-cAMP) and increasing an extracellular renoprotectant (adenosine).
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7

Cruz-Ramos, Marlid, Sara Aileen Cabrera-Nieto, Mario Murguia-Perez, and Fernanda Sarahí Fajardo-Espinoza. "The Role of Adenosine in Overcoming Resistance in Sarcomas." International Journal of Molecular Sciences 25, no. 22 (November 14, 2024): 12209. http://dx.doi.org/10.3390/ijms252212209.

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Resistance to systemic therapies in sarcomas poses a significant challenge to improving clinical outcomes. Recent research has concentrated on the tumor microenvironment’s role in sarcoma progression and treatment resistance. This microenvironment comprises a variety of cell types and signaling molecules that influence tumor behavior, including proliferation, metastasis, and resistance to therapy. Adenosine, abundant in the tumor microenvironment, has been implicated in promoting immunosuppression and chemoresistance. Targeting adenosine receptors and associated pathways offers a novel approach to enhancing immune responses against tumors, potentially improving immunotherapy outcomes in cancers, including sarcomas. Manipulating adenosine signaling also shows promise in overcoming chemotherapy resistance in these tumors. Clinical trials investigating adenosine receptor antagonists in sarcomas have fueled interest in this pathway for sarcoma treatment. Ultimately, a comprehensive understanding of the tumor and vascular microenvironments, as well as the adenosine pathway, may open new avenues for improving treatment outcomes and overcoming resistance in sarcoma. Further studies and clinical trials are crucial to validate these findings and optimize therapeutic strategies, particularly for osteosarcoma. This study provides a literature review exploring the potential role of the adenosine pathway in sarcomas.
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8

Acton, David, Matthew J. Broadhead, and Gareth B. Miles. "Modulation of spinal motor networks by astrocyte-derived adenosine is dependent on D1-like dopamine receptor signaling." Journal of Neurophysiology 120, no. 3 (September 1, 2018): 998–1009. http://dx.doi.org/10.1152/jn.00783.2017.

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Astrocytes modulate many neuronal networks, including spinal networks responsible for the generation of locomotor behavior. Astrocytic modulation of spinal motor circuits involves release of ATP from astrocytes, hydrolysis of ATP to adenosine, and subsequent activation of neuronal A1 adenosine receptors (A1Rs). The net effect of this pathway is a reduction in the frequency of locomotor-related activity. Recently, it was proposed that A1Rs modulate burst frequency by blocking the D1-like dopamine receptor (D1LR) signaling pathway; however, adenosine also modulates ventral horn circuits by dopamine-independent pathways. Here, we demonstrate that adenosine produced upon astrocytic stimulation modulates locomotor-related activity by counteracting the excitatory effects of D1LR signaling and does not act by previously described dopamine-independent pathways. In spinal cord preparations from postnatal mice, a D1LR agonist, SKF 38393, increased the frequency of locomotor-related bursting induced by 5-hydroxytryptamine and N-methyl-d-aspartate. Bath-applied adenosine reduced burst frequency only in the presence of SKF 38393, as did adenosine produced after activation of protease-activated receptor-1 to stimulate astrocytes. Furthermore, the A1R antagonist 8-cyclopentyl-1,3-dipropylxanthine enhanced burst frequency only in the presence of SKF 38393, indicating that endogenous adenosine produced by astrocytes during network activity also acts by modulating D1LR signaling. Finally, modulation of bursting by adenosine released upon stimulation of astrocytes was blocked by protein kinase inhibitor-(14–22) amide, a protein kinase A (PKA) inhibitor, consistent with A1R-mediated antagonism of the D1LR/adenylyl cyclase/PKA pathway. Together, these findings support a novel, astrocytic mechanism of metamodulation within the mammalian spinal cord, highlighting the complexity of the molecular interactions that specify motor output. NEW & NOTEWORTHY Astrocytes within the spinal cord produce adenosine during ongoing locomotor-related activity or when experimentally stimulated. Here, we show that adenosine derived from astrocytes acts at A1 receptors to inhibit a pathway by which D1-like receptors enhance the frequency of locomotor-related bursting. These data support a novel form of metamodulation within the mammalian spinal cord, enhancing our understanding of neuron-astrocyte interactions and their importance in shaping network activity.
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9

Tofovic, Stevan P., Edwin K. Jackson, and Olga Rafikova. "Adenosine deaminase–adenosine pathway in hemolysis-associated pulmonary hypertension." Medical Hypotheses 72, no. 6 (June 2009): 713–19. http://dx.doi.org/10.1016/j.mehy.2008.12.043.

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10

TINT, DIANA, CSABA KUN, ILDIKO BEKE, and ZOLTAN CSANADI. "Adenosine-Dependent Concealed Accessory Pathway." Pacing and Clinical Electrophysiology 35, no. 4 (March 21, 2011): e91-e93. http://dx.doi.org/10.1111/j.1540-8159.2011.03063.x.

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Більше джерел

Дисертації з теми "Adenosine pathway"

1

Bajracharya, Bijay. "Adenosine production via CD39/CD73 pathway promotes Leishmania amazonensis survival in macrophages." reponame:Repositório Institucional da UFOP, 2014. http://www.repositorio.ufop.br/handle/123456789/3697.

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Programa de Pós-Graduação em Ciências Biológicas. Núcleo de Pesquisas em Ciências Biológicas, Pró-Reitoria de Pesquisa e Pós Graduação, Universidade Federal de Ouro Preto.
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A leishmaniose cutânea (CL), causada por L. amazonensis, é caracterizada por uma intensa imuno- supressão e multiplicação descontrolada do parasito em modelos experimentais e é geralmente grave em humanos, variando desde a forma cutânea até a cutâneo-difusa. Não existem mecanismos precisos conhecidos sobre como L. amazonensis modula a resposta imunológica para que os macrófagos (MФ) infectados com L. amazonensis se tornem refratários à ativação por células T efetoras. Aqui, nós investigamos o possível mecanismo regulador que Leishmania provavelmente pode induzir em MФ residentes durante a interação precoce, de modo a impedir ativação das células. Neste estudo, analisou-se a expressão de CD39 e CD73, por citometria de fluxo, em MФ peritoneais murinos infectados com promastigotas metacíclicas de L. amazonensis e também a porcentagem dessas células que expressam a CD39 e CD73 foi avaliada. Nossos resultados mostraram que em 72hrs inativos os MФ tiveram baixa expressão de CD73. Curiosamente, no entanto, ao contrário de MФ tratados com LPS os infectados com L. amazonensis expressaram altos níveis de CD73. Esta informação foi posteriormente validada pelos resultados de estudos no contexto ex-vivo que mostrou igualmente que MФ infectados são predominantemente CD73+. Quando as atividades enzimáticas de CD39 e CD73 foram bloqueadas, tal como pelo uso de DIDS e MAD αβ, tanto a infecção quanto o número de amastigotas diminuiu significativamente após 48 horas de incubação. Da mesma forma, a inibição dos receptores de adenosina A2a e A2b de ZM241385 e MRS1754 também apresentou os mesmos efeitos sobre a sobrevivência do parasito e infectividade. Em estudo posterior, em busca de um possível papel da HIF- 1α na infecção por Leishmania, investigamos os efeitos da FM19G11, inibidor do HIF- 1α, na expressão de CD39 e CD73, bem como na infecção parasitária . Observou-se que, apesar de HIF - 1α poder influenciar na sobrevivência do parasito, os seus efeitos sobre a expressão de CD39 e CD73 não eram visíveis. Também foi avaliada, por PCR em tempo real, a expressão de receptores de adenosina em populações infectadas, nas quais não se observou nenhuma mudança significativa na expressão após 24 horas de infecção. Além disso, também foi avaliada a produção de citocinas, tais como TNF- α e IL-10 a partir da produção de NO nos grupos tratados. Surpreendentemente, não houve variação nos níveis destes mediadores, sugerindo a existência de outros mecanismos independentes da mediação por citocina para produção de Óxido Nítrico, tais como a produção de ROS ou efeitos leishmanacidas independentes do triptofano. Concluindo, nossos dados mostram que a infecção por L. amazonensis regula a expressão CD73 durante 24 horas de infecção e sua sobrevivência depende de atividades enzimáticas, bem como de receptores A2a e A2b. __________________________________________________________________________________________
ABSTRACT:Cutaneous leishmaniasis (CL) caused by L. amazonensis is characterized by intense immune-suppression and uncontrolled parasite multiplication in experimental models and is usually severe in humans ranging from cutaneous to diffuse cutaneous leishmaniasis. There are no precise mechanisms known how L. amazonensis modulates immune response so that macrophages (MФ) infected with L. amazonensis are refractory to activation by effector T cells. Here, we investigated the possible regulatory mechanism that Leishmania can likely induce in host MФ during early interaction so as to prevent their host cells from activation. In this study, we analyzed the expression of CD39 and CD73, by flow cytometry, in murine peritoneal MФ infected with metacyclic promastigotes of L. amazonensis and percentage of those cells expressing CD39 and CD73 was evaluated. Our results showed that 72hrs rested MФ down regulated CD73 expression. Interestingly, however, unlike LPS treated MФ, L. amazonensis infected MФ up regulated CD73 expression. This data was further validated by the findings from in ex-vivo studies which equally support that infected MФ are predominantly CD73 positive. When CD39 and CD73 enzymatic activities were blocked such as by the use of DIDS and αβ MAD, both infection and amastigote number decreased significantly within 48hrs of incubation. Similarly, inhibition of adenosine receptors A2a and A2b by ZM241385 and MRS1754 also had the same effects on the parasite survival and infection. In another study, in search of a possible role of HIF-1α in Leishmania infection, we investigated the effects of FM19G11, inhibitor of HIF-1α, on expression of CD39 and CD73 as well as parasitic infection. We observed that although HIF-1α can influence in the parasite survival, their effects on CD39 and CD73 expression were not visible. We also evaluated the expression of adenosine receptors in infected population by real time PCR in which we observed no significant change in the expression after 24hrs of infection. Moreover, we also evaluated cytokine production such as TNF-alpha, IL-10 and NO production from the treated groups. Surprisingly, there was no alternation in the levels of these mediators suggesting other mechanisms, independent of cytokine mediated nitric oxide production such as ROS production or tryptophan independent oxygen anti-leishmanacidal effects, involved in it. In conclusion, our data show that L. amazonensis infected up regulates CD73 expression during 24hrs of infection and its survival is dependent on enzyme activities as well as A2a and A2b receptors.
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2

Maiorano, Patrizia. "Adenosine Pathway as a prognostic biomarker and an actionable target to overcome “immune escape” of human tumors: the Mesothelioma model." Doctoral thesis, Università di Siena, 2022. http://hdl.handle.net/11365/1193701.

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Malignant pleural mesothelioma is an aggressive cancer and, for this disease, chemotherapy, surgery and radiotherapy are not curative. During the last years, numerous of studies have focused on immune therapies exploiting the use of immune checkpoint inhibitors. So far, these treatments are based on the use of molecules that inhibit proteins and receptors such as PD-1, PD-L1 and CTLA-4 [1]. Thus, there is the urgent need to find other immune targets. The purinergic pathway is a field of great interest as in fact there is evidence that the hypoxic environment of tumors induces increased expression of CD73 and CD39 (enzymes that produce adenosine starting from ATP) which promote the increase in extracellular adenosine [2]. High levels of adenosine are characteristic of the tumor microenvironment and induce immunosuppressive signals promoting growth and progression of tumors. For this reason [3], inhibitors of the purinergic pathway drawing attention to restore immune response to cancer cells. Our study is aimed at the identification of adenosine pathway members in MPM tissue and if this same pathway is active in this tumor. We have detected high expression of the Adenosine receptors and CD73 in MPM cells. Accordingly, treatment with the A2Br antagonist (MRS1754) provided the evidence that adenosine signaling is active in MPM cells and is a potential novel druggable target against MPM.
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3

Weyden, Louise van der. "ATP-stimulated white cell maturation via the P2Y₁₁ receptors and cAMP signaling pathway." Thesis, The University of Sydney, 2001. https://hdl.handle.net/2123/28067.

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Since the early twentieth century, biological responses to extracellular ATP have been documented in Virtually every major organ and tissue system. Our laboratory has focussed on the ability of extracellular ATP to induce elevations in the intracellular cAMP content of acute myelocytic leukaemia HL-60 cells, which subsequently results in their differentiation towards a more mature neutrophil-like cell type.
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4

Martínez, Pérez Mireya. "Involvement of the host RNA N6-adenosine methylation (m6A) pathway in the infection cycle of Alfalfa mosaic virus." Doctoral thesis, Universitat Politècnica de València, 2020. http://hdl.handle.net/10251/155976.

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[ES] Las modificaciones químicas post-transcripcionales implican un nuevo nivel de modulación de la expresión génica. Al comienzo de esta Tesis, algunos componentes del complejo de metilación del nitrógeno en posición 6 de la adenosina (m6A) habían sido caracterizados en plantas. Sin embargo, a diferencia de mamíferos y levadura, ninguno de los 13 homólogos de AlkB (atALKBH1-10B) - potenciales desmetilasas (o erasers) - y las 13 proteínas de la familia YTH (ECT1- 11, AT4G11970 y CPSF30) - potenciales proteínas de reconocimiento de m6A (o readers) - identificadas en el genoma de Arabidopsis se habían caracterizado funcionalmente. Además, varios estudios describen la presencia de m6A en RNAs de virus de mamíferos y las diferentes funciones que desempeña esta modificación en la regulación de esas infecciones. No obstante, no se ha estudiado la posible implicación de este mecanismo molecular en las infecciones virales de plantas. El descubrimiento de la interacción entre la CP del virus del mosaico de la alfalfa (AMV) y una proteína de Arabidopsis (atALKBH9B) con homología a una eraser humana fue el punto de partida de esta Tesis. En este trabajo se confirma esta interacción, y se demuestra que atALKBH9B también puede reconocer los RNAs virales. Los resultados revelan que atALKBH9B tiene la capacidad de desmetilar m6A a partir de moléculas de RNA monocatenario in vitro. Esta proteína se acumula en gránulos citoplasmáticos que se colocalizan con siRNA bodies y se asocian a P-bodies, lo que sugiere que su actividad podría estar relacionada con el silenciamiento y/o degradación de mRNA. Por otro lado, ensayos preliminares muestran que los RNAs del AMV, el virus del mosaico del pepino (CMV), el virus de la arruga del nabo (TCV) y el virus del mosaico de la coliflor (CaMV) se metilan durante la infección en Arabidopsis. Además, para AMV y CMV, los resultados fueron corroborados por UPLC-PDA-Tof-MS y los sitios m6A a lo largo de los RNAs del AMV fueron identificados mediante MeRIP-seq. Los resultados presentados confirman que la relación m6A/A a lo largo de los RNAs virales aumenta en plantas atalkbh9b en comparación con las silvestres, mientras que la traducción y/o replicación se ven afectadas y el movimiento sistémico a los tallos florales está prácticamente bloqueado. A diferencia de la CP de AMV, la de CMV no interacciona con atALKBH9B por Y2H y, como ocurre con el resto de virus analizados (CMV, TCV y CaMV), su ciclo de infección no se ve afectado en plantas atalkbh9b. Además, la secuenciación de mRNA realizada en este trabajo revela que la infección por AMV induce algunos genes de Arabidopsis pertenecientes a la maquinaria m6A, MTA, MTB, VIR y ECT5. De acuerdo con el efecto antiviral dependiente de m6A para el AMV y teniendo en cuenta que ECT2, ECT3 y ECT4 fueron recientemente caracterizadas como readers citoplasmáticas, la supresión del módulo ECT2/ECT3/ECT5 aumenta significativamente los títulos sistémicos de AMV y CMV. El efecto antiviral de ECT2 sobre AMV parece estar modulado por su unión directa a los residuos de m6A presentes en los RNAs virales, ya que un mutante de ECT2 defectuoso en el reconocimiento de m6A pierde la actividad antiviral que sí presenta la proteína original y no es capaz de arrastrar RNAs virales in vivo. Por otro lado, acorde a la localización previamente descrita para ECT2 y ECT4 y la capacidad de ECT2 para experimentar una fase similar al gel in vitro, la expresión transitoria de ECT5 muestra un patrón citoplasmático con formación de agregados. Se propone que, como se ha descrito para las proteínas YTH de mamíferos, la interacción entre las ECTs y el RNA polimetilado (en este caso, RNA viral) promovería la formación de gránulos de estrés y, en consecuencia, reduciría las tasas de traducción y replicación viral. En resumen, en este trabajo se caracteriza la primera m6A eraser de plantas, atALKBH9B, y, por primera vez, se describe la influencia del mecanismo de metilación m6A en las infecciones virales de plantas.
[EN] Post-transcriptional chemical modifications entail a new level of gene expression modulation. At the beginning of this Thesis, some components of the N6-adenosine methylation (m6A) complex had been characterized in plants, whereas 13 homologs of AlkB (atALKBH1-10B) - putative demethylases (or erasers) - and 13 proteins of the YTH family (ECT1-11, AT4G11970 and CPSF30) had been identified in the Arabidopsis genome. However, unlike mammals and yeast, no functional roles had been described for any of these proteins. Besides, several reports have brought to light the presence of m6A residues in viral RNAs from mammalian viruses and the critical roles that this modification plays regulating viral infections. However, the potential relevance of this molecular mechanism on plant viral infections remained fully unexplored. The discovery of the interaction between the AMV CP and an Arabidopsis protein (atALKBH9B) with similarity to a human eraser was the starting point of this Thesis. Here, this interaction is confirmed and it is demonstrated that atALKBH9B can also recognize the viral RNAs. Furthermore, the obtained results prove that atALKBH9B has the capability of demethylating m6A from single-stranded RNA molecules in vitro. This protein was observed to accumulate in cytoplasmic granules that colocalize with siRNA-bodies and associate to P-bodies, suggesting that atALKBH9B activity could be related to mRNA silencing and/or decay processes. On the other hand, preliminary assays show that viral RNAs of AMV, Cucumber mosaic virus (CMV), Turnip crinkle virus (TCV) and Cauliflower mosaic virus (CaMV) become methylated during infection in Arabidopsis. Besides, for AMV and CMV, the results were corroborated by UPLC-PDA-Tof-MS and m6A sites along the RNAs of AMV were identified through MeRIP-seq approach. The results presented here confirm that m6A/A ratio along viral RNAs is increased in atalkbh9b plants compared to wild type, whereas translation and/or replication are impaired and systemic movement to the floral stems is practically blocked. In contrast to AMV, CMV CP does not interact with atALKBH9B by Y2H and, as it occurs with the rest of the assayed viruses (CMV, TCV and CaMV), its infection cycle is not affected in atalkbh9b plants. Furthermore, the mRNA-seq analysis performed in this Thesis reveals that some Arabidopsis factors belonging to the m6A machinery, MTA, MTB, VIR and ECT5 genes, are upregulated upon AMV infection. Consistent with the m6A-dependent antiviral effect for AMV and considering that ECT2, ECT3 and ECT4 were recently characterized as cytoplasmic m6A readers, mutations of ECT2/ECT3/ECT5 Arabidopsis module significantly increase AMV and CMV systemic titers. The antiviral effect of ECT2 on AMV seems to be modulated via its direct binding to the m6A residues presented in the viral RNAs, since an ECT2 mutant defective in m6A recognition loses wild type antiviral activity and is not able to pull down viral RNAs in vivo. On the other hand, according to the previous subcellular localization described for ECT2 and ECT4 and the ability of ECT2 to undergo gel-like phase in vitro, the transitory expression of ECT5 displays a cytoplasmic pattern with the formation of some aggregates. As found for mammal YTH proteins, the interaction between ECTs and poly-methylated RNA (in this case viral RNA) is proposed to promote the formation of stress granules and, consequently, reduce viral translation and replication rates. In summary, in this work, atALKBH9B is reported as the first m6A eraser identified in plants and, for the first time, it is described the influence of m6A methylation mechanism in plant viral infections.
[CA] Les modificacions químiques post-transcripcionals impliquen un nou nivell de modulació de l'expressió gènica. Al començament d'esta Tesi, s'havien caracteritzat alguns components del complex de metilació del nitrogen en posició 6 de la adenosina (m6A) en plantes. No obstant això, a diferència de mamífers i llevat, cap dels 13 homòlegs d'AlkB (atALKBH1-10B) - potencials desmetilases (o erasers) - i les 13 proteïnes de la família YTH (ECT1- 11, AT4G11970 i CPSF30) - potencials proteïnes de reconeixement de m6A (o readers) - identificades en el genoma d'Arabidopsis s'havien caracteritzat funcionalment. A més, diversos estudis han descrit la presència de residus m6A en RNAs de virus de mamífers i les diferents funcions que exercix esta modificació en la regulació de les infeccions virals. No obstant això, no s'ha estudiat la possible implicació d'este mecanisme molecular en les infeccions virals de plantes. El descobriment de la interacció entre la CP del virus del mosaic de l'alfals (AMV) i una proteïna d'Arabidopsis (atALKBH9B) amb homologia a una eraser humana va ser el punt de partida d'esta Tesi. En este treball es confirma esta interacció, i es demostra que atALKBH9B també pot reconéixer els RNAs virals. Els resultats revelen que atALKBH9B té la capacitat de desmetilar m6A a partir de molècules de RNA monocatenari in vitro. Esta proteïna s'acumula en grànuls citoplasmàtics que es colocalitzen amb siRNA bodies i s'associen a P-bodies, la qual cosa suggerix que l'activitat atALKBH9B podria estar relacionada amb els processos de silenciament i/o degradació de mRNA. D'altra banda, assajos preliminars mostren que els RNAs virals de l'AMV, el virus del mosaic del cogombre (CMV), el virus de l'arruga del nap (TCV) i el virus del mosaic de la coliflor (CaMV) es metilen durant la infecció en Arabidopsis. A més, per AMV i CMV els resultats van ser confirmats per UPLC-PDA-Tof-MS i els llocs m6A al llarg dels RNAs d'AMV s'identificaren mitjançant MeRIP-seq. Els resultats presentats confirmen que la relació m6A/A al llarg dels RNAs virals augmenta en les plantes atalkbh9b en comparació amb les silvestres, mentre que la traducció i/o replicació es veuen afectades i el moviment sistèmic a les tiges florals està pràcticament bloquejat. A diferència de la CP d'AMV, la de CMV no interacciona amb atALKBH9B per Y2H i, com ocorre amb la resta dels virus analitzats (CMV, TCV i CaMV), el seu cicle d'infecció no es veu afectat en plantes atalkbh9b. A més, la seqüenciació de mRNA realitzada en este treball revela que la infecció per AMV indueix alguns gens d'Arabidopsis pertanyents a la maquinària m6A, MTA, MTB, VIR i ECT5. D'acord amb l'efecte antiviral dependent de m6A per a l'AMV i tenint en compte que ECT2, ECT3 i ECT4 van ser recentment caracteritzades com readers citoplasmàtiques, la supressió del mòdul ECT2/ECT3/ECT5 augmenta significativament els títols sistèmics d'AMV i CMV. L'efecte antiviral d'ECT2 sobre AMV sembla estar modulat a través de la seua unió directa als nucleòtids m6A presents en els RNAs virals, ja que un mutant de la proteïna ECT2 defectuós en el reconeixement de m6A perd l'activitat antiviral que sí que presenta la proteïna original i no és capaç d'arrossegar RNAs virals in vivo. D'altra banda, d'acord amb la localització subcel·lular descrita prèviament per a ECT2 i ECT4 i la capacitat d'ECT2 per a experimentar una fase similar al gel in vitro, l'expressió transitòria d'ECT5 mostra un patró citoplasmàtic amb la formació d'agregats. Es proposa que, com s'ha descrit per a les proteïnes YTH de mamífers, la interacció entre les ECTs i el RNA polimetilat (en aquest cas, RNA viral) promouria la formació de grànuls d'estrès i, en conseqüència, reduiria les taxes de traducció i replicació viral. En resum, en este treball es caracteritza la primera m6A eraser de plantes, atALKBH9B, i, per primera vegada, es descriu la influència de l'mecanisme de metilació M6A en les infeccions virals de plantes.
Martínez Pérez, M. (2020). Involvement of the host RNA N6-adenosine methylation (m6A) pathway in the infection cycle of Alfalfa mosaic virus [Tesis doctoral]. Universitat Politècnica de València. https://doi.org/10.4995/Thesis/10251/155976
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COLELLA, MARINA. "White matter injury and neuroinflammation in the developing brain: implication of adenosine pathway in clinical and pre-clinical studies." Doctoral thesis, Università degli studi di Genova, 2018. http://hdl.handle.net/11567/931189.

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Adenosine blood levels and complications of prematurity in a selected population of very low birth weight infants. We have recently reported high blood adenosine levels in extremely premature infants, positively correlating to their prematurity in function of the body weight classes. Acting via purinergic receptors, adenosine can affect different vulnerable organs including the developing brain.
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Wyatt, Amanda Wyn. "Cell signalling mechanisms involved in adenosine-induced modulation of the L-Arginine nitric oxide pathway in human fetal endothelial cells." Thesis, King's College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.270791.

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7

Lenté, Marion. "Μéthylatiοn, vοie de l'adénοsine et chοndrοsarcοmes". Electronic Thesis or Diss., Normandie, 2025. http://www.theses.fr/2025NORMC404.

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Les chondrosarcomes, tumeurs rares des os, sont considérés chimio- et radio- résistants pouvant métastaser au niveau pulmonaire. À l’heure actuelle, seule la chirurgie est le traitement de référence, cependant, elle peut être très délabrante et augmente la morbidité associée. Le but de ce travail de recherche vise à identifier de nouvelles stratégies chimiothérapeutiques pouvant être applicables aux chondrosarcomes et permettant de mieux comprendre les mécanismes tumoraux mis en place dans ces tumeurs. L’identification de ces nouvelles stratégies thérapeutiques nous a amenés à nous intéresser à la voie de l’adénosine, mais également à la méthylation des histones et notamment la méthylation de la lysine 36 de l’histone H3 (H3K36). Dans un premier temps, nous avons montré que l’utilisation d’analogues de l’adénosine, déjà utilisés en clinique, la cladribine et la clofarabine pouvaient avoir des effets antitumoraux in vitro et in vivo sur les chondrosarcomes. Ces résultats confirment ceux déjà obtenus avec un autre analogue de l’adénosine, le 3-deazaneplanocine A (DZNep). Dans un second temps, nous avons voulu comprendre par quels mécanismes d’action pouvaient fonctionner les analogues, notamment le DZNep. Nous avons donc identifié la triméthylation de H3K36 (H3K36me3) comme cible potentielle. Cependant, l’inhibition pharmacologique de la méthyltransférase responsable de H3K36me3, SETD2, par l’EZM0414 n’a montré que peu d’effets sur les chondrosarcomes. Ainsi, cette étude souligne un lien entre le métabolisme, la méthylation et la voie de l’adénosine dans les chondrosarcomes et donc un possible intérêt pour associer plusieurs molécules thérapeutiques pour traiter les chondrosarcomes
Chondrosarcomas, rare bone tumors, are considered chemo and radio-resistant and can metastasize to the lung. At present, surgery is the standard treatment, but it can be damaging and increases the associated morbidity. The aim of this research work is to identify new chemotherapeutic strategies that could be applied to chondrosarcomas and provide a better understanding of the tumor mechanisms involved in these tumors. The identification of these new therapeutic strategies led us to investigate both the adenosine pathway and histone modification, in particular the methylation of lysine 36 of histone H3 (H3K36). Firstly, we demonstrated that the use of the adenosine analogs already in clinical use, cladribine and clofarabine, could have antitumoral effects in vitro and in vivo on chondrosarcoma. These results confirm those already obtained with another adenosine analog, 3-deazaneplanocine A (DZNep). Secondly, we wanted to understand the mechanisms by which analogs, and DZNep in particular, might work. We therefore identified H3K36 trimethylation (H3K36me3) as a potential target. However, pharmacological inhibition of methyltransferase responsible for H3K36me3, SETD2, by EZM0414 showed limited effects on chondrosarcomas. Thus, this study highlights a link between metabolism, methylation and adenosine pathways in chondrosarcomas, and therefore a possible interest in combining multiple therapeutic molecules to treat chondrosarcomas
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Robinson, Alexander John. "Stimulation of the mitogen-activated protein kinase (MAPK) pathway in DDT₁MF-2 cells by adenosine A₁ receptors and histamine H₁ receptors." Thesis, Nottingham Trent University, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.252331.

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Haley, Benjamin. "A Biochemical Dissection of the RNA Interference Pathway in Drosophila melanogaster: A Dissertation." eScholarship@UMMS, 2005. https://escholarship.umassmed.edu/gsbs_diss/9.

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In diverse eukaryotic organisms, double-stranded RNA (dsRNA) induces robust silencing of cellular RNA cognate to either strand of the input dsRNA; a phenomenon now known as RNA interference (RNAi). Within the RNAi pathway, small, 21 nucleotide (nt) duplexed RNA, dubbed small interfering RNAs (siRNAs), derived from the longer input dsRNA, guide the RNA induced silencing complex (RISC) to destroy its target RNA. Due to its ability to silence virtually any gene, whether endogenous or exogenous, in a variety of model organisms and systems, RNAi has become a valuable laboratory tool, and is even being heralded as a potential therapy for an array of human diseases. In order to understand this complex and unique pathway, we have undertaken the biochemical characterization of RNAi in the model insect, Drosophila melanogaster. To begin, we investigated the role of ATP in the RNAi pathway. Our data reveal several ATP-dependent steps and suggest that the RNAi reaction comprises as least five sequential stages: ATP-dependent processing of double-stranded RNA into siRNAs, ATP-independent incorporation of siRNAs into an inactive ~360 kDa protein/RNA complex, ATP-dependent unwinding of the siRNA duplex to generate an active complex, ATP-dependent activation of RISC following siRNA unwinding, and ATP-independent recognition and cleavage of the RNA target. In addition, ATP is used to maintain 5´ phosphates on siRNAs, and only siRNAs with these characteristic 5´ phosphates gain entry into the RNAi pathway. Next, we determined that RISC programmed exogenously with an siRNA, like that programmed endogenously with microRNAs (miRNAs), is an enzyme. However, while RISC behaves like a classical Michaelis-Menten enzyme in the presence of ATP, without ATP, multiple rounds of catalysis are limited by release of RISC-produced cleavage products. Kinetic analysis of RISC suggests that different regions of the siRNA play distinct roles in the cycle of target recognition, cleavage and product release. Bases near the siRNA 5´ end disproportionately contribute to target RNA-binding energy, whereas base pairs formed by the central and 3´ region of the siRNA provide helical geometry required for catalysis. Lastly, the position of the scissile phosphate is determined during RISC assembly, before the siRNA encounters its RNA target. In the course of performing the kinetic assessment of RISC, we observed that when siRNAs are designed with regard to 'functional asymmetry' (by unpairing the 5´ terminal nucleotide of the siRNA's guide strand, i.e. the strand anti-sense to the target RNA), not all of the RISC formed was active for target cleavage. We observed, somewhat paradoxically, that increased siRNA unwinding and subsequent accumulation of single-stranded RNA into RISC led to reduced levels of active RISC formation. This inactive RISC did not act as a competitor for the active fraction. In order to characterize this non-cleaving complex, we performed a series of protein-siRNA photo-crosslinking assays. From these assays we found that thermodynamic stability and termini structure plays a role in determining which proteins an siRNA will associate with, and how association occurs. Furthermore, we have found, by means of the photo-crosslinking assays, that siRNAs commingle with components of the miRNA pathway, particularly Ago1, suggesting overlapping functions or crosstalk for factors thought to be involved in separate, distinct pathways.
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Welshhans, Kristy. "Neuronal growth cone dynamics are regulated by a nitric oxide-initiated second messenger pathway." unrestricted, 2007. http://etd.gsu.edu/theses/available/etd-09282007-114034/.

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Thesis (Ph. D.)--Georgia State University, 2007.
Vincent Rehder, committee chair; Sarah Pallas, Walter William Walthall, committee members. Electronic text (248 p. : ill. (some col.)) : digital, PDF file. Description based on contents viewed Jan. 28, 2008; title from file title page. Includes bibliographical references (p. 218-248).
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Книги з теми "Adenosine pathway"

1

Keil, Gary J. Modulation of sensory afferent procesing by endogenous spinal adenosine. 1995.

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Частини книг з теми "Adenosine pathway"

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Llyod, H. G. E., and J. Schrader. "The Importance of the Transmethylation Pathway for Adenosine Metabolism in the Heart." In Topics and Perspectives in Adenosine Research, 199–208. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-45619-0_16.

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Dey, Sumit, and Ravimohan S. Mavuduru. "Adenosine Pathway in Genitourinary Malignancies: A Promising Immunotherapeutic Target." In Biomedical Translational Research, 367–91. Singapore: Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-8845-4_19.

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Sebastião, Ana M., Sofia Cristóvão-Ferreira, and Joaquim A. Ribeiro. "Downstream Pathways of Adenosine." In Adenosine, 131–56. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-3903-5_7.

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Cavero, Icilio, Claudie Hecquet, Yasmine Djellas, Véronique Gollot-Robert, and Michel Mestre. "Activation of Cardiac Adenosine Triphosphate-Sensitive K+ Channels: An Obligatory Pathway for the Cardioprotection Afforded by Ischemic and Pharmacological Preconditioning." In Molecular and Cellular Mechanisms of Cardiovascular Regulation, 69–81. Tokyo: Springer Japan, 1996. http://dx.doi.org/10.1007/978-4-431-65952-5_7.

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Merighi, Stefania, Carolina Simioni, Rob Lane, and Adriaan P. Ijzerman. "Regulation of Second Messenger Systems and Intracellular Pathways." In A3 Adenosine Receptors from Cell Biology to Pharmacology and Therapeutics, 61–73. Dordrecht: Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-90-481-3144-0_4.

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Banerjee, Anirban, Chris B. Winter, and Alden H. Harken. "Integration of Adenosine and Noradrenergic Pathways in Cardiac Preconditioning." In Developments in Cardiovascular Medicine, 499–512. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-0455-5_32.

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7

Bianchi, Nicola, Olga Prontera, Mauro Dicuio, Sergio Concetti, Alessandra Sforza, and Giovanni Corona. "Male Sex Hormones in Andrology Today." In Practical Clinical Andrology, 251–61. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-11701-5_19.

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AbstractSeveral hormonal pathways are deeply involved in the regulation of male sexual function. Testosterone (T) is involved in the modulation of all steps of sexual response from the activation (sexual desire) to the resolution (orgasm and ejaculation). Androgen receptors are deeply expressed in several brain areas involved in the control of sexual response as well as in the male genitalia tract and corpora cavernosa. At these levels, T plays a crucial role in all pathways of penile erection, including nitric oxide (NO) production and degradation, adenosine signaling, calcium sensitization, and penile smooth muscle differentiation. In addition, T is also involved in the control of ejaculatory reflex modulating male genitalia tract contractility and semen bolus expulsion. The role of other sex steroids is more limited, although estrogens seem to partially regulate male sexual desire. Thyroid system is mainly involved in the control of the ejaculatory reflex, although a possible contribution in the modulation of sexual desire and penile erection has also been supposed. Available evidence suggests that prolactin (PRL) acts in the control of sexual desire either through indirect (inducing secondary hypogonadism) or direct mechanisms (modulating dopamine and serotonin central pathways). The role of other hormonal pathways in the regulation of male sexual response appears negligible.
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Novío, Silvia, María Jesús Núñez-Iglesias, and Manuel Freire-Garabal. "Adenosine Signaling Pathways as Potential Therapeutic Targets in Prostate Cancer Disease." In Molecular Oncology: Underlying Mechanisms and Translational Advancements, 93–107. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-53082-6_4.

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Kaczmarek, Elzbieta. "Nucleotides and Novel Signaling Pathways in Endothelial Cells: Possible Roles in Angiogenesis, Endothelial Dysfunction and Diabetes Mellitus." In Extracellular ATP and Adenosine as Regulators of Endothelial Cell Function, 15–37. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-3435-9_2.

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Papachristodoulou, Despo, Alison Snape, William H. Elliott, and Daphne C. Elliott. "An alternative pathway of glucose oxidation: the pentose phosphate pathway." In Biochemistry and Molecular Biology. Oxford University Press, 2018. http://dx.doi.org/10.1093/hesc/9780198768111.003.0018.

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This chapter examines the pentose phosphate pathway, which is a pathway of glucose oxidation which does not generate adenosine triphosphate (ATP) nor oxidize a molecule of glucose completely. The chapter considers the pentose phosphate pathway as a versatile pathway that produces ribose-5-phosphate for nucleotide synthesis, supplies nicotinamide adenine dinucleotide phosphate hydrogen (NADPH) for fat synthesis and other reductive systems, and provides a route for the metabolism of surplus pentose sugars coming from the diet. The pathway has an oxidative section converting glucose-6-phosphate into ribose-5-phosphate and it produces NADPH. The chapter explores how the nonoxidative section manipulates ribose-5-phosphate according to the needs of the cell. If a cell requires equal amounts of ribose-5-phosphate and NADPH, only the oxidative section is required.
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Тези доповідей конференцій з теми "Adenosine pathway"

1

Chiarella, Anna M., and Rustgi K. Rustgi. "Abstract A06: Elucidation of the extracellular adenosine pathway in metastatic pancreatic cancer." In Abstracts: AACR Special Conference on Pancreatic Cancer: Advances in Science and Clinical Care; September 6-9, 2019; Boston, MA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.panca19-a06.

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Stellrecht, C., S. Shentu, V. Gandhi, and V. Gandhi. "The Ribonucleoside Analog, 8-Chloro-Adenosine, Inhibits the mTOR Pathway and Induces Autophagy." In Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-6116.

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Oliva, Jacqueline, Younghee Lee, Rebeca Rodriguez, Katarzyna Tomczak, Davis Ingram, Xiao Zhou, Vinod Ravi, et al. "1042 The dual function of the adenosine pathway in the liposarcoma tumor microenvironment." In SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.1042.

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Fons, Pierre, Michael Esquerré, Stéphanie Versluys, Gigliola Mambrini, Michael Paillasse, Andy Bell, Adrian Schreyer, et al. "Abstract 3970: Targeting the adenosine immunosuppressive pathway for cancer immunotherapy with small molecule agents." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-3970.

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Borker, P. V., B. Macatangay, B. Morris, A. Morris, S. M. Nouraie, X. Chen, and S. R. Patel. "Obstructive Sleep Apnea May Impact Inflammation in People With HIV Though the Adenosine Pathway." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a4453.

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Szajnik-Szczepanski, Marta E., Magdalena Derbis, Michal Lach, Paulina Patalas, Marcin Michalak, Hanna Drzewiecka, Marta Glura, Ewa Nowak-Markwitz, Marek Spaczynski, and Theresa L. Whiteside. "Abstract A79: The adenosine pathway in ovarian carcinoma: Tumor cells and tumor-derived exosomes express CD39 and CD73 ectonucleotidases, produce adenosine and mediate immune suppression." In Abstracts: AACR Special Conference on Advances in Ovarian Cancer Research: From Concept to Clinic; September 18-21, 2013; Miami, FL. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1078-0432.ovca13-a79.

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Poncelet, Lauranne, Rima Ait-Belkacem, Bruno Gomes, and Jonathan Stauber. "Abstract B048: A Promising Pathway in Immuno-oncology: CD73-Adenosine axis highlighted by quantitative mass spectrometry imaging." In Abstracts: AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics; October 26-30, 2019; Boston, MA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1535-7163.targ-19-b048.

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Poncelet, Lauranne, Rima Ait-Belkacem, Bruno Gomes, Stefan Linehan, and Jonathan Stauber. "Abstract 5485: A promising pathway in immuno-oncology: CD73-adenosine axis highlighted by quantitative mass spectrometry imaging." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-5485.

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Qiao, L., J. Zhao, and R. Wu. "Cupping Therapy Alleviates Acute Lung Injury Through the Adenosine/A2BAR Signalling Pathway in Rats." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a1079.

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Yuan, Tai-Yi, Hanan N. Fernando, Jessica Czamanski, Chong Wang, Wei Yong Gu, and Chun-Yuh Huang. "Effects of Static Compression on Energy Metabolism of Porcine Intervertebral Disc." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19600.

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Анотація:
Degeneration of the intervertebral disc (IVD) has been associated with low back pain, which is one of the major socio-economic problems in the United States. Since IVD is the largest avascular cartilaginous structure in the human body, poor nutrient supply has been suggested as a potential mechanism for IVD degeneration. Biosynthesis of extracellular matrix is an energy demanding process which is required to maintain tissue integrity [1]. Cells consume glucose and oxygen to produce adenosine triphosphate (ATP), the main energy form in cells. Glycolysis, the primary metabolic pathway for production of ATP in IVD cells, is strongly regulated by local oxygen concentration and pH (which is governed by lactate concentration) [2]. Therefore, energy metabolism may play an important role in the malnutrition pathway leading to IVD degeneration. The objective of this study was to investigate the effect of mechanical loading on cellular energy metabolism in whole disc and in agarose gels.
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Звіти організацій з теми "Adenosine pathway"

1

Osathanon, Thanaphum. Gene expression profile of continuous and intermittent compressive stress treated human periodontal ligament cells. Faculty of Dentistry Chulalongkorn University, 2019. https://doi.org/10.58837/chula.res.2019.7.

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Анотація:
Mechanical force regulates periodontal ligament cell (PDL) behavior. However, different force types lead to distinct PDL responses. Here, we report that pretreatment with an intermittent compressive force (ICF), but not a continuous compressive force (CCF), promoted human PDL (hPDL) osteogenic differentiation as determined by osteogenic marker gene expression and mineral deposition in vitro. ICF-induced osterix (OSX) expression was inhibited by cycloheximide and monensin. Although CCF and ICF significantly increased extracellular adenosine triphosphate (ATP) levels, pretreatment with exogenous ATP did not affect hPDL osteogenic differentiation. Gene expression profiling of hPDLs subjected to CCF or ICF revealed that extracellular matrix (ECM)-receptor interaction, focal adhesion, and transforming growth factor beta (TGF- β) signaling pathway genes were commonly upregulated, while calcium signaling pathway genes were downregulated in both CCF- and ICF-treated hPDLs. The TGFB1 mRNA level was significantly increased, while those of TGFB2 and TGFB3 were decreased by ICF treatment. In contrast, CCF did not modify TGFB1 expression. Inhibiting TGF- β receptor type I or adding a TGF- β1 neutralizing antibody attenuated the ICF-induced OSX expression. Exogenous TGF- β1 pretreatment promoted hPDL osteogenic marker gene expression and mineral deposition. Additionally, pretreatment with ICF in the presence of TGF- β receptor type I inhibitor attenuated the ICF-induced mineralization. In conclusion, this study reveals the effects of ICF on osteogenic differentiation in hPDLs and implicates TGF- β signaling as one of its regulatory mechanism.
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