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Статті в журналах з теми "Receptor depletion"
Frey, A. B. "Role of host antigen receptor-bearing and antigen receptor-negative cells in immune response to rat adenocarcinoma 13762." Journal of Immunology 156, no. 10 (May 15, 1996): 3841–49. http://dx.doi.org/10.4049/jimmunol.156.10.3841.
Повний текст джерелаRay, P. E., E. Castren, E. J. Ruley, and J. M. Saavedra. "Different effects of sodium or chloride depletion on angiotensin II receptors in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 258, no. 4 (April 1, 1990): R1008—R1015. http://dx.doi.org/10.1152/ajpregu.1990.258.4.r1008.
Повний текст джерелаAoh, Quyen L., Anna M. Castle, Charles H. Hubbard, Osamu Katsumata, and J. David Castle. "SCAMP3 Negatively Regulates Epidermal Growth Factor Receptor Degradation and Promotes Receptor Recycling." Molecular Biology of the Cell 20, no. 6 (March 15, 2009): 1816–32. http://dx.doi.org/10.1091/mbc.e08-09-0894.
Повний текст джерелаLu, Justine P., Yuan Wang, Danielle A. Sliter, Margaret M. P. Pearce, and Richard J. H. Wojcikiewicz. "RNF170 Protein, an Endoplasmic Reticulum Membrane Ubiquitin Ligase, Mediates Inositol 1,4,5-Trisphosphate Receptor Ubiquitination and Degradation." Journal of Biological Chemistry 286, no. 27 (May 24, 2011): 24426–33. http://dx.doi.org/10.1074/jbc.m111.251983.
Повний текст джерелаLièvremont, Jean-Philippe, Gary St J. Bird, and James W. Putney. "Canonical transient receptor potential TRPC7 can function as both a receptor- and store-operated channel in HEK-293 cells." American Journal of Physiology-Cell Physiology 287, no. 6 (December 2004): C1709—C1716. http://dx.doi.org/10.1152/ajpcell.00350.2004.
Повний текст джерелаKyakumoto, S., R. Kurokawa, and M. Ota. "Mechanism of replenishment of androgen receptors in cytosol of mouse submandibular gland." Journal of Endocrinology 115, no. 3 (December 1987): 411–18. http://dx.doi.org/10.1677/joe.0.1150411.
Повний текст джерелаPeterson, Theresa J., Sudipan Karmakar, Margaret C. Pace, Tong Gao та Carolyn L. Smith. "The Silencing Mediator of Retinoic Acid and Thyroid Hormone Receptor (SMRT) Corepressor Is Required for Full Estrogen Receptor α Transcriptional Activity". Molecular and Cellular Biology 27, № 17 (25 червня 2007): 5933–48. http://dx.doi.org/10.1128/mcb.00237-07.
Повний текст джерелаLinas, S. L., R. Marzec-Calvert, and M. E. Ullian. "K depletion alters angiotensin II receptor expression in vascular smooth muscle cells." American Journal of Physiology-Cell Physiology 258, no. 5 (May 1, 1990): C849—C854. http://dx.doi.org/10.1152/ajpcell.1990.258.5.c849.
Повний текст джерелаMorris, Gavin E., Carl P. Nelson, Paul J. Brighton, Nicholas B. Standen, R. A. John Challiss, and Jonathon M. Willets. "Arrestins 2 and 3 differentially regulate ETA and P2Y2 receptor-mediated cell signaling and migration in arterial smooth muscle." American Journal of Physiology-Cell Physiology 302, no. 5 (March 1, 2012): C723—C734. http://dx.doi.org/10.1152/ajpcell.00202.2011.
Повний текст джерелаClarke, David C., Meredith L. Brown, Richard A. Erickson, Yigong Shi та Xuedong Liu. "Transforming Growth Factor β Depletion Is the Primary Determinant of Smad Signaling Kinetics". Molecular and Cellular Biology 29, № 9 (17 лютого 2009): 2443–55. http://dx.doi.org/10.1128/mcb.01443-08.
Повний текст джерелаДисертації з теми "Receptor depletion"
Khoboko, Thabelo. "Effect of age and unilateral dopamine depletion on striatal NMDA receptor function." Master's thesis, University of Cape Town, 2005. http://hdl.handle.net/11427/3409.
Повний текст джерелаCasali, Brad Thomas. "Disease-Modifying Effects of Microglia Depletion and Nuclear Receptor Deletion inMyeloid Cells in Alzheimer's Disease." Case Western Reserve University School of Graduate Studies / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=case1599047858196611.
Повний текст джерелаHughes, Simon Anthony. "Role of membrane PIP2 hydrolysis and depletion in receptor-induced inhibition of potassium M(Kv7)channels." Thesis, University College London (University of London), 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.506810.
Повний текст джерелаThoma, Michelle C. "Regulating the regulators using CD25 depletion to enhance immune responses to a model plasmid-based vaccine /." Diss., Columbia, Mo. : University of Missouri-Columbia, 2008. http://hdl.handle.net/10355/5764.
Повний текст джерелаThe entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. "August 2008" Includes bibliographical references.
Beiko, Jason. "The effect of nonspatial water maze pretraining in rats subjected to serotonin depletion and muscarinic receptor antagonism, a detailed behavioural assessment of spatial performance." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0008/MQ28540.pdf.
Повний текст джерелаTirelle, Pauline. "Role du microbiote intestinal dans la régulation de l'axe intestin-cerveau au cours du modèle murin d'anorexie " activity-based anorexia Gut microbiota alteration in a mouse model of Anorexia Nervosa Comparison of different modes of antibiotic delivery on gut microbiota depletion efficiency and body composition in mouse Gut microbiota depletion affects nutritional and bahavioral responses to activity-based anorexia model in a sex-dependent manner Invalidation of Toll-like receptor 4 in intestinal epithelial cells modifies the response to activity base anorexia model in a sex-dependent manner." Thesis, Normandie, 2020. http://www.theses.fr/2020NORMR056.
Повний текст джерелаAnorexia nervosa (AN) is an eating disorder (ED) with female predominance, mainly characterised by a decrease of food intake leading to a severe body weight loss. Furthermore, psychiatric comorbidities are frequently observed in AN patients such as depression and anxiety. During the last decade, the role of microbiota-gut-brain axis in ED and anxiety-like behavior has emerged. Several studies reported gut microbiota dysbiosis in anorectic patients. Nevertheless, the pathophysiology of AN remains poorly understood. The aim of the present PhD thesis was to better understand the contribution of the gut microbiota in the regulation of gut-brain axis in the mouse model of anorexia "activity-based anorexia" (ABA). The ABA model combines spontaneous physical activity with a free running wheel access and a progressive limited food access. In a first study, we characterised the gut microbiota of C57Bl/6 male mice submitted to ABA model. We observed in ABA mice an increase of Lactobacillus and clostridium cocleatum belonging to genus of Clostridium, as well as a decrease of Burkholderiales. Interestingly, correlations between bacteria taxa and food intake, body weight and body composition have been observed. Then, we aimed to evaluate the response to ABA model of mice with gut microbial depletion. We thus compared in a second study different dosing and administration of large spectrum antibiotic treatments, either by oral gavages (once or twice a day) or by addition in drinking water. Although these three strategies led to a strong decrease of faecal bacteria, once day oral gavage induced proliferation of Gammaproteobacteria. Thus, antibiotics administration by oral gavage twice a day or in drinking water appear as the most appropriate modes to achieve gut microbiota depletion. In a third study, we then evaluated the response to ABA model of both male and female C57Bl/6 mice with antibiotic-induced microbiota depletion. Firstly, we observed that antibiotic administration led to an increase of fat mass and a decrease of lean mass. During the ABA model, gut microbiota-depleted mice exhibited a lower decrease of body weight compared to untreated ABA mice. In males, we also observed altered anxiety-like behavior in ABA mice with depleted gut microbiota. We thus showed that gut microbiota-depleted mice exhibited an altered response to ABA model in a sex-dependent manner. Finally, in order to decipher the underlying mechanisms, we focused on toll-like receptor 4 (TLR4), an endogenous receptor of lipopolysaccharides. Previous studies suggested TLR4 implication in the regulation of feeding and anxiety-like behaviors. To determine the involvement of intestinal TLR4, we submitted mice with intestinal epithelial TLR4 knockout to the ABA model. Again, we observed a sex-dependent response: a delayed and limited body weight loss in males and an increase of anxiety-like behavior in females. In conclusion, studies performed during this PhD thesis highlight the alterations and the role of gut microbiota in the activity-based anorexia model that appear to be sex-dependent
Ritsou, Elena. "The role of CD4 and CXCR4 mediated apoptosis in T cell depletion during HIV-1 infection." Thesis, Open University, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.390903.
Повний текст джерелаFávero, Michele Thaís. "Respostas cardiorrespiratórias promovidas pela ativação de receptores glutamatérgicos e purinérgicos no núcleo do trato solitário." Universidade Federal de São Carlos, 2012. https://repositorio.ufscar.br/handle/ufscar/1341.
Повний текст джерелаFinanciadora de Estudos e Projetos
The central nervous system (CNS) has an important role in maintaining the composition and volume of body fluids for the appropriate tissue perfusion. An important area of the CNS that receives cardiorespiratory afferents is the nucleus of the solitary tract (NTS) that has several types of neurotransmitters, includingL-glutamate and adenosine 5'-triphosphate (ATP). Neuroendocrine changes that occur during sodium depletion could change glutamatergi c and purinergic neurotransmissions into the NTS. Thus, in this study, we investigated : 1) the effects of sodium depletion on cardiorespiratory responses before and after injections of L -glutamate and α,β-methyleneadenosine 5′-triphosphate (α,β-methyl ATP, a selective P2X purinergic receptor agonist) into the NTS of unanesthetized and sodium depleted rats; 2) the cardiorespiratory responses of the injection of α,β-methyl ATP before and after the blockade of P2 receptor purinergic antagonist with suramin (non-selective P2 purinergic receptor antagonist) into NTS of unanesthetized and normovolemic rats and 3) to describe the autonomic components involved with the cardiovascular responses after injection of α,β-methyl ATP into the NTS. Male Holtzman rats with a cannula implanted into the NTS and catheters inserted into the femoral artery and vein were used. Ventilation (VE) was measured by whole body plethysmograph method. In relation to objective 1, the cardiorespiratory parameters were measured in normovolemic (before sodium depletion), depleted (24 h after sodium depletion) and repleted rats (two hours after free access to 0.3 M NaCl and water). Sodium depletion was induced by the treatment with the diuretic furosemide (20 mg/kg of body weight) injected subcut aneously (s.c.) followed by 24 h of sodium -deficient diet. Sodium depletion did not modify baseline MAP (104 ± 4 mmHg, vs. normovolemic: 105 ± 4 mmHg) or HR (334 ± 20 bpm, vs. normovolemic: 379 ± 13 bpm) but increased the VE (708 ± 107 ml/min/kg, vs. normovolemic: 478 ± 60 ml/min/kg). This effect was due to increase on tidal volume (VT, 7 ± 0.6 ml/kg, vs. normovolemic: 5 ± 0.4 ml/kg) without effect on the respiratory frequency (fR, 99 ± 8 cpm, vs. normovolemic: 85 ± 6 cpm). In repleted rats, VE did not return to normal level (640 ± 33 ml/min/kg, vs. normovolemic: 478 ± 60 ml/min/kg). Unilateral injections of L-glutamate (1 and 5 nmol/100 nl) into the NTS produced pressor response (17 ± 3 and 36 ± 3 mmHg, respectively, vs. saline: 3 ± 1 mmHg), bradycardia (-130 ± 15 and -169 ± 10 bpm, respectively, vs. saline: -13 ± 6 bpm) and the hyperventilation (233 ± 44 and 495 ± 114 ml/min/kg, respectively, vs. saline: 32 ± 26 ml/min/kg). Sodium depletion reduced pressor responses (4 ± 3 mmHg and 13 ± 4 mmHg, respectively) and hyperventilation (-112 ± 112 and 7 ± 115 ml/min/kg, respectively) and did not change bradycardia (-116 ± 30 and -156 ± 18 bpm, respectively). Unilateral injections of α,β-methyl ATP (2 nmol/100 nl) into the NTS also produced pressor response (36 ± 5 mmHg, vs. saline: 3 ± 1 mmHg), bradycardia (-194 ± 18 bpm, vs. saline: -13 ± 6 bpm) and did not change VE (54 ± 96 ml/min/kg, vs. saline: 32 ± 26 ml/min/kg). Sodium depletion reduced pressor response (24 ± 5 mmHg), VE ( -147 ± 184 ml/min/kg) and did not change bradycardia (-168 ± 22 bpm). In relation to objective 2, the results showed that injection of α,β-methyl ATP (2 nmol/100 nl) into NTS produced pressor response (24 ± 4 mmHg e -187 ± 39 bpm, respectively) and these responses were reduced 15 min after injection of suramin into NTS ipsilateral (13 ± 2 mmHg e -80 ± 18 bpm). Injection of α,β-methyl ATP into NTS produced no significantly change in VE. In relation to objective 3, the results showed that injection of α,β-methyl ATP (2 nmol/100 nl) into NTS promote pressor and bradycardic response (32 ± 5 mmHg and -183 ± 21 bpm). The pre-treatment with the alpha1 -adrenoceptor antagonist prazosin (1 mg/kg bw, i.v.) attenuated the increase in MAP (+10 ± 3 mmHg) without changing the bradycardic response (-192 ± 21 bpm) evoked by injection of α,β-methyl ATP into NTS. The pre-treatment with the cholinergic muscarinic antagonist, methyl-atropine (1 mg/kg bw, i.v.) did not changed the pressor response (+31 ± 6 mmHg) and abolished the bradycardic response (+21 ± 6 bpm) induced by injection of α,β-methyl ATP into the NTS. The results suggest that neuroendocrine changes produced by sodium depletion (increased level of circulating ANG II, aldosterone and the desactivation of the volume receptors and baroreceptors) may change the glutamatergic and purinergic neurotransmissions into the NTS. Furthermore, activation of P2X receptors in the NTS activates both the sympathetic and parasympathetic nervous system to produce pressor and bradycardic responses, respectively, without changing ventilation
O sistema nervoso central (SNC) possui um papel fundamental na manutenção da composição e do volume dos líquidos corporais, para a adequada perfusão tecidual. Uma importante área do SNC que recebe aferências cardiorrespiratórias é o núcleo do trato solitário (NTS) que possui vários tipos de neurotransmissores, dentre eles o L-glutamato e adenosina-5´-trifosfato (ATP). Mudanças neuroendócrinas que ocorrem durante a depleção de sódio poderiam alterar as neurotransmissões glutamatérgica e purinérgica no NTS. Assim, neste estudo, tivemos 3 objetivos: 1) investigar os efeitos da depleção de sódio nas respostas cardiorrespiratórias antes e após a injeção de L-glutamato e α,β-metileno adenosina 5’ trifosfato (α,β-metil ATP, agonista seletivo de receptor purinérgico P2X) no NTS de ratos não anestesiados; 2) investigar as respostas cardiorrespiratórias à injeção de α,β-metil ATP no NTS antes e após o bloqueio dos receptores purinérgicos P2 com o suramin (antagonista não-seletivo de receptores P2) no NTS de ratos não anestesiados e normovolêmicos e 3) caracterizar os componentes autonômicos envolvidos nas respostas cardiovasculares após a injeção de α,β-metil ATP no NTS. Foram utilizados ratos Holtzman com cânulas implantadas no NTS e com cateter inserido na artéria e veia femoral. As medidas de ventilação (VE) foram obtidas pelo método de pletismografia de corpo inteiro. Com relação ao objetivo 1, os parâmetros cardiorrespiratórios foram medidos em ratos normovolêmicos (antes da depleção de sódio), depletados (24 h após a depleção de sódio) e ratos repletos (2 h após o livre acesso a NaCl 0,3 M e água). A depleção de sódio foi induzida pelo tratamento com o diurético furosemida (20 mg/Kg do peso corporal) injetado subcutaneamente (s.c.) acompanhado de uma dieta deficiente em sódio por 24 h. A depleção de sódio não modificou a PAM basal (104 ± 4 mmHg, vs. normovolêmicos: 105 ± 4 mmHg) nem a FC (334 ± 20 bpm, vs. normovolêmico: 379 ± 13 bpm) mas aumentou a VE (708 ± 107 ml/min/kg, vs. normovolêmico: 478 ± 60 ml/min/kg). Este efeito ocorreu devido a um aumento do volume corrente (VC, 7 ± 0,6 ml/kg, vs. normovolêmico: 5 ± 0,4 ml/kg) sem alterar a frequência respiratória (fR, 99 ± 8 cpm, vs. normovolêmicos: 85 ± 6 cpm). Em ratos repletos, a VE não retornou ao nível normal (640 ± 33 ml/min/kg vs. normovolêmico: 478 ± 60 ml/min/kg). Injeções unilaterais de Lglutamato (1 e 5 nmol/100 nl) no NTS produziu resposta pressora (17 ± 3 e 36 ± 3 mmHg, respectivamente, vs. salina: 3 ± 1 mmHg), bradicardia (-130 ± 15 e -169 ± 10 bpm, respectivamente, vs. salina: -13 ± 6 bpm) e hiperventilação (233 ± 44 e 495 ± 114 ml/min/kg, respectivamente, vs. salina: 32 ± 26 ml/min/kg). A depleção de sódio reduziu a resposta pressora (4 ± 3 mmHg e 13 ± 4 mmHg, respectivamente) e hiperventilação (-112 ± 112 e 7 ± 115 ml/min/kg, respectivamente) e não alterou a bradicardia (-116 ± 30 e -156 ± 18 bpm, respectivamente). Injeção unilateral de α,β-metil ATP (2 nmol/100 nl) no NTS também produziu resposta pressora (36 ± 5 mmHg, vs. salina: 3 ± 1 mmHg), bradicardia (- 194 ± 18 bpm, vs. salina: -13 ± 6 bpm) e não modificou a VE (54 ± 96 ml/min/kg, vs. salina: 32 ± 26 ml/min/kg). A depleção de sódio reduziu a resposta pressora (24 ± 5 mmHg), a VE (-147 ± 184 ml/min/kg) e não alterou a bradicardia (-168 ± 22 bpm). Com relação ao objetivo 2, os resultados mostraram que a injeção de α,β-metil ATP (2 nmol/100 nl) no NTS promoveu resposta pressora e bradicárdica (24 ± 4 mmHg e -187 ± 39 bpm, respectivamente) e estas respostas foram reduzidas aos 15 minutos após a injeção de suramin no NTS ipsilateral (13 ± 2 mmHg e -80 ± 18 bpm). A injeção de α,β-metil ATP no NTS não promoveu alterações significativas na VE. Com relação ao objetivo 3, os resultados mostraram que as injeções de α,β-metil ATP (2 nmol/100 nl) no NTS promoveu resposta pressora e bradicardia (+32 ± 5 mmHg e -183 ± 21 bpm). O pré-tratamento com o antagonista de receptor alfa-1 adrenérgico, prazosin (1 mg/kg de peso corporal, i.v.), atenuou o aumento da PAM (+10 ± 3 mmHg) sem alterar a bradicardia (-192 ± 21 bpm) provocada pela injeção de α,β-metil-ATP no NTS e o pré-tratamento com o antagonista colinérgico muscarínico, metil-atropina (1 mg/kg de peso corporal, i.v.) não alterou a resposta pressora (+31 ± 6 mmHg) e aboliu a bradicardia (+21 ± 6 bpm) induzida pela injeção de α,β-metil ATP no NTS. Os resultados sugerem que alterações neuroendócrinas produzidas pela depleção de sódio (aumento dos níveis de ANG II e aldosterona circulantes e a desativação de receptores de volume e dos barorreceptores) podem alterar as neurotransmissões glutamatérgica e purinérgica no NTS. Além disso, a ativação dos receptores purinérgicos P2X no NTS ativa simultaneamente o sistema nervoso simpático e parassimpático para produzir respostas pressora e bradicárdica, respectivamente, sem alterar a ventilação pulmonar.
Engelschalt, Vivienne. "Mechanismen der antikörpervermittelten T-Zell-Depletion in vivo im Maus-Modell." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2010. http://dx.doi.org/10.18452/16234.
Повний текст джерелаMonoclonal antibodies (mAb) are efficiently used for the therapeutic depletion of various cells in vivo yet the mechanisms of depletion are still unclear. In this work, the molecular principles of CD4+ T cell depletion (CD4 Tcd) by a single application of 100 µg of the anti-CD4 mAb YTS191.1.1 were investigated in the mouse. A strong correlation between the depletion and the surface modulation of the CD4 molecule could be observed. At the same time, organ-dependent differences in the kinetics as well as in the efficiency of depletion could be detected. In the thymus, neither modulation nor depletion were detectable. In the spleen and the lymph nodes (Ln), the modulation was strong and the depletion was maximal (80-90%) 48 h after mAb treatment. Interestingly, both modulation and depletion were decreased and delayed (50-60% after 72 h) in the Peyer`s patches. By using C3-deficient mice, no major contribution of complement to the CD4 Tcd was seen. On the contrary, with the help of different FcGamma-receptor (FcGammaR)-deficient mice (FcGammaRI, FcGammaRII, FcGammaRIII, FcGammaRI/III, and FcRGamma) and through the blockade of FcGammaRIV, a strong organ dependent involvement of FcGammaR could be shown. While the depletion in the spleen was clearly dependent on FcGammaRIV, in the Ln and the Peyer`s patches, FcGammaRI/III were involved. These findings correlated with the strong expression of FcGammaRIV in the spleen, the lung, the colon, the kidney, and the liver, while in the Ln the expression was weak and undetectable in the thymus and the Peyer`s patches. For the first time, F4/80high macrophages in the spleen could be identified as also being FcGammaRIV+, and are therfore considered as the potential effector cells of the CD4 Tcd. The direct comparison of the depletion of T cells via CD4 or ICOS pointed out that the target cell depletion is not only dependent on the properties of the mAb used, but also on those of the target molecule.
Tavares, Lucas Alves. "O envolvimento da proteína adaptadora 1 (AP-1) no mecanismo de regulação negativa do receptor CD4 por Nef de HIV-1." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/17/17136/tde-06012017-113215/.
Повний текст джерелаThe Human Immunodeficiency Virus (HIV) is the etiologic agent of Acquired Immunodeficiency Syndrome (AIDS). AIDS is a disease which has a global distribution, and it is estimated that there are currently at least 36.9 million people infected with the virus. During the replication cycle, HIV promotes several changes in the physiology of the host cell to promote their survival and enhance replication. The fast progression of HIV-1 in humans and animal models is closely linked to the function of an accessory protein Nef. Among several actions of Nef, one is the most important is the down-regulation of proteins from the immune response, such as the CD4 receptor. It is known that this action causes CD4 degradation in lysosome, but the molecular mechanisms are still incompletely understood. Nef forms a tripartite complex with the cytosolic tail of the CD4 and adapter protein 2 (AP-2) in clathrin-coated vesicles, inducing CD4 internalization and lysosome degradation. Previous research has demonstrated that CD4 target to lysosomes by Nef involves targeting of this receptor to multivesicular bodies (MVBs) pathway by an atypical mechanism because, although not need charging ubiquitination, depends on the proteins from ESCRTs (Endosomal Sorting Complexes Required for Transport) machinery and the action of Alix, an accessory protein ESCRT machinery. It has been reported that Nef interacts with subunits of AP- 1, AP-2, AP-3 complexes and Nef does not appear to interact with AP-4 and AP-5 subunits. However, the role of Nef interaction with AP-1 or AP-3 in CD4 down-regulation is poorly understood. Furthermore, AP-1, AP-2 and AP-3 are potentially heterogeneous due to the existence of multiple subunits isoforms encoded by different genes. However, there are few studies to demonstrate if the different combinations of APs isoforms are form and if they have distinct functional properties. This study aim to identify and characterize cellular factors involved on CD4 down-modulation induced by Nef from HIV-1. More specifically, this study aimed to characterize the involvement of AP-1 complex in the down-regulation of CD4 by Nef HIV-1 through the functional study of the two isoforms of ?-adaptins, AP-1 subunits. By pull-down technique, we showed that Nef is able to interact with ?2. In addition, our data from immunoblots indicated that ?2- adaptin, not ?1-adaptin, is required in Nef-mediated targeting of CD4 to lysosomes and the ?2 participation in this process is conserved by Nef from different viral strains. Furthermore, by flow cytometry assay, ?2 depletion, but not ?1 depletion, compromises the reduction of surface CD4 levels induced by Nef. Immunofluorescence microscopy analysis also revealed that ?2 depletion impairs the redistribution of CD4 by Nef to juxtanuclear region, resulting in CD4 accumulation in primary endosomes. Knockdown of ?1A, another subunit of AP-1, resulted in decreased cellular levels of ?1 and ?2 and, compromising the efficient CD4 degradation by Nef. Moreover, upon artificially stabilizing ESCRT-I in early endosomes, via overexpression of HRS, internalized CD4 accumulates in enlarged HRS-GFP positive endosomes, where co-localize with ?2. Together, the results indicate that ?2-adaptin is a molecule that is essential for CD4 targeting by Nef to ESCRT/MVB pathway, being an important protein in the endo-lysosomal system. Furthermore, the results indicate that ?-adaptins isoforms not only have different functions, but also seem to compose AP-1 complex with distinct cell functions, and only the AP-1 variant comprising ?2, but not ?1, acts in the CD4 down-regulation induced by Nef. These studies contribute to a better understanding on the molecular mechanisms involved in Nef activities, which may also help to improve the understanding of the HIV pathogenesis and the related syndrome. In addition, this work contributes with the understanding of primordial process regulation on intracellular trafficking of transmembrane proteins.
Книги з теми "Receptor depletion"
Cheung, Hermia. Effect of dopamine depletion on D1 receptor binding in rat brain; and metabolism studies of D1 agonist R-[11C]SKF 82957 and phosphodiesterase-4 inhibitor R-[11C}rolipram. Ottawa: National Library of Canada, 2003.
Знайти повний текст джерелаЧастини книг з теми "Receptor depletion"
Cheng, Kwong Tai, Hwei Ling Ong, Xibao Liu, and Indu S. Ambudkar. "Contribution of TRPC1 and Orai1 to Ca2+ Entry Activated by Store Depletion." In Transient Receptor Potential Channels, 435–49. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-94-007-0265-3_24.
Повний текст джерелаKitic, Maja, Peter See, Julia Bruttger, Florent Ginhoux, and Ari Waisman. "Novel Microglia Depletion Systems: A Genetic Approach Utilizing Conditional Diphtheria Toxin Receptor Expression and a Pharmacological Model Based on the Blocking of Macrophage Colony-Stimulating Factor 1 Receptor." In Microglia, 217–30. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9658-2_16.
Повний текст джерелаCaetano Crowley, Fabiana A., Bryan Heit, and Stephen S. G. Ferguson. "Super-Resolution Imaging of G Protein-Coupled Receptors Using Ground State Depletion Microscopy." In Methods in Molecular Biology, 323–36. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9121-1_18.
Повний текст джерелаAbi-Dargham, Anissa, Larry Kegeles, Mark Slifstein, and Marc Laruelle. "Chapter 24 Antipsychotic-Induced Changes in Striatal D2 Receptors in Schizophrenia: In Vivo Evidence from Dopamine Depletion Studies." In Staging Neuropsychiatric Disorders, 259–64. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-1-4614-0785-0_24.
Повний текст джерелаAbi-Dargham, Anissa, Larry Kegeles, Mark Slifstein, and Marc Laruelle. "Chapter 27 Antipsychotic-Induced Changes in Striatal D2 Receptors in Schizophrenia: In Vivo Evidence from Dopamine Depletion Studies." In Staging Neuropsychiatric Disorders, 293–98. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7264-3_27.
Повний текст джерелаPeters, Maximilian, Ben Katz, Shaya Lev, Rachel Zaguri, Rita Gutorov, and Baruch Minke. "Depletion of Membrane Cholesterol Suppresses Drosophila Transient Receptor Potential-Like (TRPL) Channel Activity." In Sterol Regulation of Ion Channels, 233–54. Elsevier, 2017. http://dx.doi.org/10.1016/bs.ctm.2017.05.005.
Повний текст джерелаBernard, Véronique, Corinne Brana, Isabel Liste, Oksana Lockridge, and Bertrand Bloch. "Dramatic depletion of cell surface muscarinic receptor due to limited delivery from intracytoplasmic stores in neurons of acetylcholinesterase-deficient mice." In Cholinergic Mechanisms, 477–79. CRC Press, 2004. http://dx.doi.org/10.3109/9780203493878-71.
Повний текст джерелаToro-Urrego, Nicolas, Marco Avila-Rodriguez, María Inés Herrera, Andrea Aguilar, Lucas Udovin, and Juan P. Luaces. "Neuroactive Steroids in Hypoxic–Ischemic Brain Injury: Overview and Future Directions." In Neuroprotection - New Approaches and Prospects. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.93956.
Повний текст джерела"MAGNESIUM DEPLETION INDUCES HYPERCALCEMIA IN D3 REPLETE AND UP REGULATION OF THE INTESTINAL l,25(OH)2D3 RECEPTOR IN DDEPLETED RATS." In Vitamin D, 718–19. De Gruyter, 1991. http://dx.doi.org/10.1515/9783110850345-244.
Повний текст джерелаSaikarthik, Jayakumar, Ilango Saraswathi, and Abdulrahman A. Al-Atram. "Does COVID-19 Affect Adult Neurogenesis? A Neurochemical Perspective." In Recent Advances in Neurochemistry [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.101179.
Повний текст джерелаТези доповідей конференцій з теми "Receptor depletion"
Gossage, David L., Michel Laviolette, Gail M. Gauvreau, Richard Leigh, Roland Kolbeck, Yanping Wu, Laura Richman, and Nestor A. Molfino. "Depletion Of Airway Eosinophils By Benralizumab An Anti-IL5 Receptor Alpha Monoclonal Antibody." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a3961.
Повний текст джерелаO'Brien, Sarah A., Katarzyna Skrzypczynska, Jessica Orf, Brian Belmontes, Hong Tan, Daniel Lu, Ian Driver, and Jackson Egen. "Abstract 2803: CSF-1 receptor-mediated macrophage depletion can induce immunomodulatory resistance mechanisms in murine tumor models." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-2803.
Повний текст джерелаO'Brien, Sarah A., Katarzyna Skrzypczynska, Jessica Orf, Brian Belmontes, Hong Tan, Daniel Lu, Ian Driver, and Jackson Egen. "Abstract 2803: CSF-1 receptor-mediated macrophage depletion can induce immunomodulatory resistance mechanisms in murine tumor models." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-2803.
Повний текст джерелаFidanza, Mario, Sumin Jo, Arnawaz Bashir, Stephan A. Grupp, Alix E. Seif, and Gregor S. Reid. "Abstract B33: Toll-like receptor ligands delay acute lymphoblastic leukemia onset via depletion of pre-leukemic cells." In Abstracts: AACR Special Conference: Pediatric Cancer at the Crossroads: Translating Discovery into Improved Outcomes; November 3-6, 2013; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.pedcan-b33.
Повний текст джерелаAchyut, B. R., David A. Bader, Hannah H. Yan, Chaoyang Li, Yanli Pang, and Li Yang. "Abstract 3969: Stromal depletion of transforming growth factor receptor 2 promotes the development of forestomach squamous cell carcinoma." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-3969.
Повний текст джерелаSkrzypczynska, Katarzyna M., Sarah A. O'Brien, Brian Belmontes, Hong Tan, Jessica Orf, Daniel Lu, Ian Driver, and Jackson G. Egen. "Abstract A71: Resistance mechanisms limiting the immunostimulatory and antitumor activity of anti-CSF-1 receptor-mediated macrophage depletion." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 27-30, 2018; Miami Beach, FL. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm18-a71.
Повний текст джерелаScharf, R. E., M. Stockschläder, H. J. Reimers, and W. Schneider. "THE REDUCED CAPACITY OF THROMBOXANE FORMATION IN THROMBIN-PREACTIVATED PLATELETS IS NOT CAUSED BY DEPLETION OF THEIR ARACHIDONIC ACID POOL." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643393.
Повний текст джерелаWachtfogel, Yanina T., Peter C. Harpel, L. Henry Edmunds, and Robert W. Colman. "FORMATION OF Cl -Cl INHIBITOR AND KALLIKREIN-Cl INHIBITOR COMPLEXES DURING CARDIOPULMONARY BYPASS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642900.
Повний текст джерелаGastaldello, Gabriel Henrique, Amanda Rodrigues Correia Frota Gomes, Bruna Belone Garcia, Damiana Gianotto Pires, and Cristiane Tefé Sillva. "Pathogenesis and clinical aspects involved in stroke associated with COVID-19: A literature review." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.611.
Повний текст джерелаSharma, Naveen, and James P. Allison. "Abstract B143: Fc gamma receptor IV mediated depletionof tumor infiltrating regulatory T cells by anti-CTLA4 antibody is promoted byTLR1/2 agonist and hence its efficacy in anti-tumor combination therapy." In Abstracts: Second CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 25-28, 2016; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6066.imm2016-b143.
Повний текст джерелаЗвіти організацій з теми "Receptor depletion"
Savaldi-Goldstein, Sigal, and Todd C. Mockler. Precise Mapping of Growth Hormone Effects by Cell-Specific Gene Activation Response. United States Department of Agriculture, December 2012. http://dx.doi.org/10.32747/2012.7699849.bard.
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