Добірка наукової літератури з теми "Metabolic CD34+ cells"
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Статті в журналах з теми "Metabolic CD34+ cells":
Fadini, G. P. "Circulating CD34+ cells, metabolic syndrome, and cardiovascular risk." European Heart Journal 27, no. 18 (August 9, 2006): 2247–55. http://dx.doi.org/10.1093/eurheartj/ehl198.
Kochi, Yu, Yoshikane Kikushige, Toshihiro Miyamoto, and Koichi Akashi. "Identification of ASCT1 As a Candidate Molecule Enhancing Antioxidant Activity in Primary Human AML Cells." Blood 128, no. 22 (December 2, 2016): 1674. http://dx.doi.org/10.1182/blood.v128.22.1674.1674.
Nakasone, Hideki, Misato Kikuchi, Yu Akahoshi, Koji Kawamura, Miki Sato, Kazuki Yoshimura, Yukiko Misaki, et al. "The Expression of CD83 Would be Increased in CD34-Positive Monocytes Detected in Peripheral Blood Mobilized By G-CSF in Humans." Blood 132, Supplement 1 (November 29, 2018): 2063. http://dx.doi.org/10.1182/blood-2018-99-112084.
Desterke, Christophe, Estelle Balducci, Xavier Fund, Claire Borie, Annelise Bennaceur-Griscelli, and Ali G. Turhan. "A Novel Metabolic Transcriptome Identified in Myelodysplastic Syndromes (MDS) Correlates with OMS Classification and Poor Prognosis." Blood 132, Supplement 1 (November 29, 2018): 5495. http://dx.doi.org/10.1182/blood-2018-99-110678.
Perrone, Olivia, Tiziana Coppola, James Bartram, Waseem Nasr, Juying Xu, and Marie-Dominique Filippi. "The Effect of SCD-1 Inhibition on Human Hematopoietic Stem Cell Mitochondrial Metabolism, Cell Proliferation, and Differentiation Potential." Blood 142, Supplement 1 (November 28, 2023): 1308. http://dx.doi.org/10.1182/blood-2023-185260.
Devaraj, Sridevi, and Ishwarlal Jialal. "Dysfunctional Endothelial Progenitor Cells in Metabolic Syndrome." Experimental Diabetes Research 2012 (2012): 1–5. http://dx.doi.org/10.1155/2012/585018.
Dalloul, Ali H., Claire Patry, Jean Salamero, Bruno Canque, Fernanda Grassi, and Christian Schmitt. "Functional and Phenotypic Analysis of Thymic CD34+CD1a− Progenitor-Derived Dendritic Cells: Predominance of CD1a+ Differentiation Pathway." Journal of Immunology 162, no. 10 (May 15, 1999): 5821–28. http://dx.doi.org/10.4049/jimmunol.162.10.5821.
Nishida, Yuki, Edward Ayoub, Darah Scruggs, Shayaun Khazaei, Faryal Munir, Lauren B. Ostermann, Po Yee Mak, et al. "Stem-Cell Enriched Cellular Hierarchy of TP53 Mutant Acute Myeloid Leukemia Is Vulnerable to Targeted Protein Degradation of c-MYC." Blood 142, Supplement 1 (November 28, 2023): 583. http://dx.doi.org/10.1182/blood-2023-174938.
Rai, Richa, Foramben Patel, Stella Melana, Jonathan Feld, Shyamala C. Navada, Rosalie Odchimar-Reissig, Erin P. Demakos, E. Premkumar Reddy, and Lewis R. Silverman. "Rigosertib in Combination with Azacitidine Impacts Metabolic and Differentiation Pathways in the MDS-L Cell Line." Blood 136, Supplement 1 (November 5, 2020): 35–36. http://dx.doi.org/10.1182/blood-2020-142908.
Forte, Dorian, Roberto Maria Pellegrino, Francesco Fabbri, Ivan Vannini, Samantha Bruno, Giulia Corradi, Rafael J. Argüello, et al. "Circulating Extracellular Vesicles from Acute Myeloid Leukemia Patients Drive Distinct Metabolic Profile of Leukemic Cells and Reveal Crucial Lipidomic Biomarkers." Blood 138, Supplement 1 (November 5, 2021): 3471. http://dx.doi.org/10.1182/blood-2021-150339.
Дисертації з теми "Metabolic CD34+ cells":
Guimarães, Tânia Maria Rocha 1963. "Perfil de expressão de células progenitoras endoteliais circulantes CD45-/ CD34+/KDR+ em mulheres hipertensas na pré-menopausa em comparação com mulheres saudáveis normotensas = Expression profile of circulating endothelial progenitor cells CD45-/ CD34+/KDR+ in hypertensive premenopausal women compared with healthy normotensive women." [s.n.], 2014. http://repositorio.unicamp.br/jspui/handle/REPOSIP/317311.
Tese (doutorado) - Universidade Estadual de Campinas, Instituto de Biologia
Made available in DSpace on 2018-08-26T00:13:01Z (GMT). No. of bitstreams: 1 Guimaraes_TaniaMariaRocha_D.pdf: 3499853 bytes, checksum: 2767ae0d1bab61dda96ce4765cd63588 (MD5) Previous issue date: 2014
Resumo: As células progenitoras endoteliais (EPCs) estão envolvidas em neovasculogênese e na manutenção da homeostase vascular, sua deficiência pode ter papel na patogênese da hipertensão. Este estudo teve como objetivo analisar o perfil de expressão das EPCs circulantes e diferentes fatores de risco cardiovascular em mulheres hipertensas, na pré-menopausa, em comparação com mulheres normotensas saudáveis. Realizou-se um estudo caso-controle com 45 mulheres voluntárias, faixa etária de 30 a 50 anos (41 ± 6) no Ambulatório do Pronto Socorro Cardiológico de Pernambuco. As EPCs definidas como CD45-/CD34+/KDR+ foram coletadas em sangue venoso periférico e analisadas por citometria de fluxo. As mulheres foram classificadas como controles (CT) saudáveis normotensas com PAS (pressão arterial sistólica) < 130 mmHg e PAD (pressão arterial diastólica) < 85 mmHg (n=15), com hipertensão primária: a) Leve (HL) PAS=140-159mm Hg e PAD=90-99 mmHg (n=15) e b) Severa (HS) PAS > 180 mmHg e PAD > 110 mmHg (n=15). Os grupos foram entrevistados quanto aos hábitos de fumo, prática de exercícios físicos e Índice de Massa Corporal (IMC), sendo aferido o nível da PA em repouso. Realizou-se análise nos prontuários dos resultados dos exames séricos de colesterol total, lipoproteínas de alta densidade-colesterol (HDL-c), lipoproteínas de baixa densidade-colesterol (LDL-c), triglicerídeos e glicemia de jejum, no mês da coleta das amostras sanguíneas. Os resultados comprovaram redução significativa ao número de EPCs no HL (74%) e HS (88%) versus CT; e redução de 67% no HS versus HL, evidenciando relação inversa entre o número de células e o estágio da hipertensão. O grupo HS apresentou aumento de 49% de células CD45+ demonstrando padrão inflamatório e redução de 61% de CD45-/CD34+. Quanto aos níveis séricos verificou-se: HDL-c [HL (52±7); HS (48±5)]; LDL-c [HL (130±8); HS (143±15)]; triglicerídeos [HL (138±19); HS(153 ±40)]; glicemia de jejum [HL(95±7);HS(121±39)] e IMC [HL(31±4);HS(29±3)]; revelando que 67% das mulheres com hipertensão severa apresentavam síndrome metabólica (SM). O desenvolvimento da hipertensão e da SM foi diretamente correlacionado com a diminuição das EPCs. Portanto, a contagem de EPCs pode ser considerada um marcador biológico adequado para indicar a gravidade do estado hipertensivo em mulheres
Abstract: Endothelial progenitor cells (EPCs) are involved in neovasculogenesis and maintenance of vascular homeostasis and their impairment may have a role in the pathogenesis of hypertension. This study aimed analyzes the expression profile of circulating EPCs and different cardiovascular risk factors in hypertensive premenopausal women compared with healthy normotensive women. A case-control study was conducted enrolling 45 women volunteers, aged from 30- 50 years (41 ± 6) in Ambulatory of the Cardiologic Emergency Hospital of Pernambuco. EPCs numbers were determined by flow cytometry in peripheral blood as the CD45-/CD34+/KDR+ cells. The women were classified as healthy normotensive controls (CT) with SBP (systolic blood pressure) <130 mmHg and DBP (diastolic blood pressure) < 85 mmHg (n=15), and with essential hypertension; a) mild (MH), SBP=140-159 mmHg and DBP=90-99 mmHg (n=15); and b) severe (SH), SBP>180 mmHg and DBP>110 mmHg (n=15). The group were interviewed regarding smoking habits, physical exercise and body mass index (BMI), and measured the level of blood pressure at quiescent. An analysis in records of test results cholesterol, high density lipoprotein-cholesterol (HDL-c), low density lipoprotein-cholesterol (LDL-c), triglycerides and fasting glucose in the month of collection of blood samples. The results found a significant reduction in circulating EPCs numbers in MH (74%) and SH (88%) when compared to the CT and reduction of 67% in SH when compared to MH, an inverse relationship between the number of cells and the stage of hypertension. SH group showed an increase of 49% CD45+ cells demonstrating inflammation and reduction of 61% CD45-/ CD34+ cells. Regarding the biochemical serum was found: HDL-c [MH (52±7); SH (48±5)]; LDL-c [MH (130±8); SH (143±15)]; triglycerides [MH (138±19); SH (153±40)]; fasting glucose [MH (95±7); SH (121±39)] and BMI [MH (31±4); SH (29±3)]; revealing that 67% of women with severe hypertension had metabolic syndrome (MS). Development of hypertension and the parameters related to MS are directly correlated with a decrease of circulating EPCs. Therefore, the EPCs counting may be considered a suitable biological marker to follow up the evolution of the hypertensive state in women
Doutorado
Biologia Celular
Doutora em Biologia Celular e Estrutural
Refeyton, Alice. "La survie et les adaptations métaboliques des cellules primitives mésenchymateuses et hématopoïétiques en anoxie et anoxie/aglycémie." Electronic Thesis or Diss., Bordeaux, 2024. http://www.theses.fr/2024BORD0028.
Mesenchymal stromal cells (MStroC) comprise multipotent stem cells (SC) capable of regenerating tissues damaged by ischemic insults. However, high mortality of MStroC after transplantation is highlighted during their engraftment. Therefore, exploring strategies to improve the viability of cell grafts constitutes the challenge of cell therapy. To this end, we performed functional and metabolic analyzes on two different types of populations containing somatic SC: MStroC and a population of hematopoietic niche partner cells, CD34+.MStroC or CD34+ cells were cultured under conditions of anoxia (absence of O2) and ischemic type (anoxia/aglycemia, absence of O2 and glucose, AA) or at 3% O2 corresponding to the physiological optimal concentration, then analyzed.Functional assays reveal that MStroC and CD34+ cells exhibit complete proliferation and differentiation properties in anoxia. Functional analyzes of single cells and gene expression revealed that MStroC and CD34+ are not only maintained in an AA state, but are those in which SC, having the highest proliferation and differentiation capacity, are the most enriched. Multiparametric metabolic analysis shows that survival in anoxia is mainly supported by glycolysis and lipid metabolism. On the other hand, the energy homeostasis of MStroC in the AA condition is partially ensured by anaerobic mitochondrial activity particularly involving mitochondrial complexes I, III and ubiquinone. Furthermore, a significant accumulation of succinate in this condition for both types of SC was demonstrated. This is due in part to an inversion of succinate dehydrogenase, which in turn is driven by fumarate spillover from purine nucleotide degradation and malate-aspartate shuttle activity. However, major pathways contributing to succinate accumulation include glycogen-induced glucose/pyruvate stimulation, as well as ketone body, amino acid, and propanoate metabolism which provide succinyl-CoA converted to succinate. Furthermore, MStroC ischemia survival is linked to sulfide metabolism and H2S consumption, as well as improved survival in the presence of H2S donors. SQR-mediated H2S oxidation results in reverse electron transport at mitochondrial complex I, using glutathione as an electron acceptor. The analysis of the use of energy substrates showed that CD34+ cells in anoxia seem to mainly use simple sugars in order to fuel the glycolytic pathway and a consequent reduction in mitochondrial metabolism compared to the 3% O2 condition. In contrast, in AA, Krebs cycle intermediates are used intensively to provide the coenzyme NAD/NADH.Our results reveal a great metabolic flexibility of MStroC and CD34+ populations based on the enrichment of somatic SC detected in anoxia or in the condition mimicking ischemia. Thus, unlike differentiated cells, somatic SC (mesenchymal and hematopoietic) have the capacity to survive in conditions of anoxia and aglycemia using the evolutionary conservative energy pathways existing in early eukaryotes living in anoxic zones enriched in sulfide . Exploiting this ex vivo conditioning under conditions mimicking ischemia could constitute a strategy to improve the survival of MStroC implanted in hypoxic/ischemic tissues
Zancanaro, Krauss Maria Eduarda. "CD4+ T cell metabolism during Trichuris muris infection." Thesis, University of Manchester, 2018. https://www.research.manchester.ac.uk/portal/en/theses/cd4-t-cell-metabolism-during-trichuris-muris-infection(24eb0cc7-db70-46ea-ba49-e4fe3d5a5d03).html.
St-Pierre, Jessica. "The role of CD4⁺ Foxp3⁺ naturally-occurring regulatory T cells in the host immune response to Plasmodium chabaudi AS /." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111941.
Tripmacher, Robert. "Untersuchungen zu Wirkungen einer eingeschränkten Energiesynthese auf Funktionen von humanen Immunzellen." Doctoral thesis, Humboldt-Universität zu Berlin, Medizinische Fakultät - Universitätsklinikum Charité, 2005. http://dx.doi.org/10.18452/15260.
Background: The function of immune cells is dependent upon a constant and adequate supply of energy. Energy is formed via OXPHOS in the mitochondria and via cytosolic glycolysis. Oxygen and glucose are the main substrates for energy synthesis. Objective: In severe diseases or in inflamed areas cellular energy supply is significantly impaired due to inadequate supply of cellular microenvironment with oxygen and nutrients. The aim of this study was to answer the question, whether and how human immune cells maintain viability and functional activity under these circumstances. Methods: Human CD4+ T cells and CD14+ monocytes were isolated by MACS from peripheral blood of healthy donors. The extent of oxidative energy formation was determined via measurement of oxygen consumption using a Clark type electrode. Energy production was restricted in glucose-free cell culture medium and by gradually inhibited OXPHOS using myxothiazol. T cell proliferation was flow-cytometrically analysed using CFDA SE after stimulation with CD3 and CD28 antibodies. Cytokine synthesis was assessed by flow-cytometrical immunofluorescence and the paraformaldehyde-saponin procedure after stimulation of T cells with PMA/ionomycin in the presence of brefeldin A. Phagocytosis of monocytes was measured using a commercial test system (FACS technique). HIF-1alpha expression was assessed by semiquantitative PCR and immunoblot after the stimulation of myxothiazol treated T cells with PMA/ionomycin. Results: In glucose-containing medium all investigated immune functions were unaffected even under complete suppression of OXPHOS. Only when OXPHOS and glycolysis were simultaneously and almost completely suppressed a significant decrease was found. Glucose deprivation per se caused both a significantly reduced proliferation and phagocytosis. It is supposed, that T cells are able to compensate for an energy deficit by an excess of oxygen consumption and strongly induced glycolysis. However, HIF-1alpha was found to be not crucial for switching to anaerobic energy synthesis. Conclusion: These data quantify the energy requirement of functional activity in highly purified human immune cell fractions. An unexpectedly high adaptive potential of immune cells to maintain specific functions even under massively impaired energetic conditions could be demonstrated.
COMPAGNONE, MIRCO. "ΔNp63 controls hyaluronic acid metabolism and signaling in head and neck squamous cell carcinoma". Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2015. http://hdl.handle.net/2108/202937.
p63 is a transcription factor belonging to the p53 family. Like other members of the p53 family, the TP63 gene is expressed as multiple isoforms arising by either alternative promoter usage or differential splicing events at the C-terminus. Particularly, the ΔN proteins, although lack the canonical transcriptional activation domain, are endowed with an alternative transactivation domain and promote cancer cell survival and tumor progression in squamous cell carcinomas (SCCs) of different origins. By combining RNA-seq approach with co-expression studies in human primary tumors, we identified and characterized the hyaluronan synthase 3 (Has3), the hyaluronidase 1 and 3 (Hyal1 and 3), and CD44 as novel ∆Np63 regulated genes. Has3 catalyzes the synthesis of hyaluronic acid (HA), while Hyal1 and Hyal3 catalyze the degradation of HA. CD44 is the main signal-transducing HA plasma membrane receptor. We found that in HNSCC cell lines of different origin, ∆Np63 silencing decreased Has3 expression and concomitantly increased the expression of Hyal1 and Hyal3, resulting in the inhibition of the extracellular level of HA. Mechanistically, we found that ∆Np63 directly bound to and activated the promoter of Has3 and, conversely, bound to the promoter and the 3’-terminal region of Hyal3 and 1, respectively, resulting in the repression of gene expression. Accordingly, in several primary squamous tumor datasets, we found that the expression of p63 was positively correlated with that of Has3. HA-mediated signaling is mediated through its interaction with plasma membrane receptors, including primarily CD44. We found that in tumor cells, ∆Np63 silencing decreased CD44 expression and, accordingly, the expression of p63 was positively correlated with that of CD44 in primary squamous tumor data sets. Mechanistically, we found that ∆Np63 directly bound to and activated the promoter of CD44. HA-CD44 interaction is important for mediating chemoresistance by sustaining the full activation of several tyrosine kinase receptors (EGFR, ErbB2 and IGFR) and promoting the expression of ABC drug transporters. We found that ∆Np63, through its action on HA metabolism and CD44 abundance, regulated the tyrosine kinase receptors activation and ABC drug transporter expression, mediating thus, tumor chemoresistance. Notably, in vitro ∆Np63-depletion, similar to Has3 silencing and HA-synthesis inhibition by 4-MU treatment, reduced cancer cell chemoresistance, indicating the ∆Np63 ability to promote chemoresistance in a HA-dependent manner. Moreover, in different human tumors data sets, the positive correlation between p63 and Has3 expression was a negative prognostic factor on HNSCC patient survival, suggesting that the ΔNp63/HA signaling axis is an important determinant of the p63-driven tumorigenesis.
Divoux, Jordane. "Etude du métabolisme des lymphocytes T CD4+ Foxp3+ régulateurs à l’homéostasie et dans un contexte inflammatoire." Thesis, Sorbonne université, 2019. https://accesdistant.sorbonne-universite.fr/login?url=http://theses-intra.upmc.fr/modules/resources/download/theses/2019SORUS075.pdf.
CD4+ Foxp3+ regulatory T cells (Treg) are able to control the activity of the immune system and are essential to maintain immune tolerance. These cells are thus beneficial in autoimmune diseases while their anti-inflammatory action promotes tumor growth. Understanding Treg biology is therefore a major axis for the development of new therapeutic strategies applicable to these two types of pathologies. In this work we investigated Treg metabolism as information available to date are still controversial. In contrast to conventional T cells (Tconv), which use anabolic metabolism under the control of mTOR, Treg are today considered as catabolic cells with a metabolism favored by AMPK. In order to test this hypothesis, we used conditional knock out mice allowing gene deletion of AMPK or mTOR, specifically in Treg. The study of these mice highlight an unsuspected role of mTOR in the stability and migration of Treg as well as an involvement of AMPK in the ability of Treg to inhibit anti-tumor response. This work puts in question current considerations on Treg metabolism and opens the way towards a better understanding of the metabolism of these cells at homeostasis and in pathological context
Vahlas, Zoï. "Régulation métabolique de l'infection des cellules T CD4 par VIH-1 : vers de nouvelles cibles thérapeutiques." Thesis, Montpellier, 2020. http://www.theses.fr/2020MONTT009.
The susceptibility of CD4 T cells to HIV-1 infection is regulated by glucose and glutamine metabolism, but the relative contributions of these nutrients to infection are not known. During my PhD, I identified glutaminolysis as a major pathway fueling oxidative phosphorylation (OXPHOS) in activated naïve as well as memory CD4 cell subsets, and found that induction of this metabolic network is required for optimal HIV-1 infection. Moreover, we determined that under conditions of attenuated glutaminolysis, the α-ketoglutarate (αKG) TCA (tricarboxylic acid) cycle intermediate is a rate-limiting step in infection; exogenous α-KG directly increased OXPHOS and rendered both naïve and memory CD4 T cells significantly more sensitive to infection. Furthermore, blocking the glycolytic flux of pyruvate to lactate resulted in an increased OXPHOS and a significantly augmented level of HIV-1 infection. In agreement with these data, infected CD4 T cells exhibited increased mitochondrial biomass and respiration as compared to their non-infected counterparts. These data identify the OXPHOS/ aerobic glycolysis balance as a major regulator of HIV-1 infection in CD4 T lymphocytes.In order to gain more insight into the metabolic pathways regulating HIV-1 infection in CD4 T cells, we developed a complementary approach to target upstream processes, specifically altering glucose (GLUT1), glutamine (ASCT2), and arginine (CAT1) transporter expression by lentiviral-mediated delivery of specific shRNAs. Testifying to the importance of these transporters, CD4 T cells with downregulated expression of either GLUT1, ASCT2 or CAT1 were negatively selected, resulting in a loss of approximately 80% of shRNA-transduced cells within 14 days. Notably, the permissivity of CD4 T cells to HIV-1 infection was differentially impacted by inhibition of specific nutrient transporters. Consistent with the data presented above, knockdown of GLUT1 did not significantly impact HIV-1 infection whereas knockdown of CAT1 significantly decreased both OXPHOS as well as HIV-1 infection (by 35%). Surprisingly though, ASCT2 knockdown resulted in a significantly augmented infection, by approximately 20%. Mechanistically, we found that this was associated with a markedly higher persistence of naïve, as compared to memory, T cells with downregulated ASCT2 levels. These data highlight differences in the relative importance of distinct nutrient transporters in the survival of naïve vs memory CD4 T cell subsets and demonstrate their specific impact on the sensitivity of these populations to HIV-1 infection.In conclusion, using two complementary approaches, my PhD research has revealed the critical impact of a CD4 T cell’s energetic state on its susceptibility to HIV-1 infection. My data identify the importance of mitochondrial metabolism, with an environment rich in TCA cycle intermediates such as α-KG, in regulating the susceptibility of CD4 T cells to HIV-1 infection. Furthermore, I find that nutrient transporter expression differentially impacts the sensitivity of naïve and memory CD4 T cells to HIV-1 infection. These studies therefore provide new prospects for the development of targeted metabolic therapeutic strategies against HIV-1 infection
Aroua, Nesrine. "Etude in vivo de la chimiorésistance dans les leucémies aigues myéloïdes humaines." Thesis, Toulouse 3, 2018. http://www.theses.fr/2018TOU30369.
Acute myeloid leukemia (AML) is the most common adult leukemia characterized by clonal expansion of immature myeloblasts. Despite a high rate of complete remission after conventional front-line induction chemotherapy (e.g. daunorubicin or idarubicin plus cytarabine), the prognosis is very poor in AML. This unfavorable overall survival is caused by frequent relapses due to chemoresistant leukemic cell populations (RLCs) in AML. RLCs are thought to be enriched in quiescent leukemic stem/immature cells (LSCs). However, these hypotheses have never been tested directly in vivo. My PhD work was devoted to validate this hypothesis in vivo. We first developed a clinically relevant chemotherapeutic approach treating patient derived xenografts (PDX) with cytarabine (AraC) to characterize AraC residual cells. AraC-treated AML cells are not necessarily enriched for neither immature cells or quiescent (G0) cells or leukemic initiating cells (LICs). Rather chemotherapy resistant cells in vivo have high levels of reactive oxygen species (ROS), showed increased mitochondrial mass, and retained active mitochondria, consistent with a high oxidative phosphorylation (OxPHOS) status. AraC residual cells exhibited increased fatty acid oxidation and a high OxPHOS gene signature predictive for treatment response in PDX and patients. Treatment of High OxPHOS but not Low OxPHOS human AML cell lines demonstrated chemotherapy resistance in vivo. Targeting mitochondrial metabolism induced an energetic shift toward low OxPHOS status and markedly enhanced antileukemic effects of AraC in AML. In the second part of my PhD study, we identified ecto-nucleoside triphosphate diphosphohydrolase-1 CD39 (ENTPD1) overexpressed in RLCs in vivo after chemotherapy. We confirmed that AraC increased cell surface CD39 expression in AML cell lines in vitro and in vivo as well as in 24 diverse PDX models. We further observed this increase in 50 patients at 35-days post-intensive chemotherapy compared to their respective diagnosis. Interestingly, high CD39 expression on AML patients was associated with a worse response to AraC in vivo. We furthermore demonstrated that CD39 downstream signaling pathway was dependent on cAMP-PKA axis and its inhibition by H89 sensitized AML cells to AraC through the inhibition of PGC1a, TFAM and mitochondrial OxPHOS function.[...]
Bishop, Kenneth D. "Egr-2 and PD-1 Are Required for Induction and Maintenance of T Cell Anergy: A Dissertation." eScholarship@UMMS, 2005. https://escholarship.umassmed.edu/gsbs_diss/354.
Книги з теми "Metabolic CD34+ cells":
Workshop on Mechanisms and Specificity of HIV Entry into Host Cells (1989 San Francisco, Calif.). Mechanisms and specificity of HIV entry into host cells. New York: Plenum Press, 1991.
Düzgünes, Nejat. Mechanisms and Specificity of HIV Entry into Host Cells. Springer London, Limited, 2012.
Düzgünes, Nejat. Mechanisms and Specificity of HIV Entry into Host Cells. Springer, 1991.
Düzgünes, Nejat. Mechanisms and Specificity of HIV Entry into Host Cells. Springer, 2012.
Частини книг з теми "Metabolic CD34+ cells":
Matsumoto, Kengo, Ken-ichi Hirano, Shuichi Nozaki, Makoto Nishida, Takeshi Ohya, Mohamed Janabi Yakub, Tohru Funahashi, Shizuya Yamashita, and Yuji Matsuzawa. "Expression of CD36 in Cultured Human Aortic Smooth Muscle Cells (HASMCs)." In Lipoprotein Metabolism and Atherogenesis, 272–74. Tokyo: Springer Japan, 2000. http://dx.doi.org/10.1007/978-4-431-68424-4_59.
Bossi, Paolo, and Erika Stucchi. "Exercise and Nutrition Interventions in Head and Neck Cancer." In Critical Issues in Head and Neck Oncology, 347–54. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-23175-9_21.
Sugano, Ryo, Mariko Harada-Shiba, Noriyasu Nishimura, Yasuko Miyake, Jun An, Dong Xan Hui, Taku Yamamura, and Akira Yamamoto. "CD36 Expression in Human Monocytic Leukemia Cell Lines: THP-1 and THP-1 Subtype, Show Different Expressions of Type I and Type II Scavenger Receptors." In Lipoprotein Metabolism and Atherogenesis, 230–32. Tokyo: Springer Japan, 2000. http://dx.doi.org/10.1007/978-4-431-68424-4_49.
Gordon-Smith, E. C., and Emma C. Morris. "Haemopoietic stem cell transplantation." In Oxford Textbook of Medicine, edited by Chris Hatton and Deborah Hay, 5579–88. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0549.
Wu, Hongmin, and Xiancai Zhong. "Nrf2 as a therapy target for Th17-dependent autoimmune disease." In The Role of NRF2 Transcription Factor [Working Title]. IntechOpen, 2024. http://dx.doi.org/10.5772/intechopen.1005037.
A. Rakityanskaya, Irina, Tat’jana S. Ryabova, Anastasija A. Kalashnikova, Goar S. Balasaniants, Andrej D. Kaprin, Feliks I. Ershov, Vera V. Kir’janova, et al. "Perspective Chapter: The Role of Interferon Gamma in Clinical Medicine." In Interferon - Immune Metabolism [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.105476.
Masson, Jesse James Ronald, and Clovis Steve Palmer. "Glucose metabolism in CD4 and CD8 T cells." In Molecular Nutrition: Carbohydrates, 129–47. Elsevier, 2019. http://dx.doi.org/10.1016/b978-0-12-849886-6.00016-1.
Gould, Kathleen L. "Cyclin-dependent protein kinases." In Protein Kinase Functions, 277–302. Oxford University PressOxford, 2000. http://dx.doi.org/10.1093/oso/9780199637713.003.0010.
Тези доповідей конференцій з теми "Metabolic CD34+ cells":
Shen, Yao-An, Yau-Huei Wei, and Yann-Jang Chen. "Abstract 482: High CD44/CD24 expressive cells presented cancer stem cell characteristics and undergo mitochondrial resetting and metabolic shift in nasopharyngeal carcinoma." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-482.
Dimitriu, Gabriel, Vasile lucian Boiculese, Mihaela Moscalu, and Cristina gena Dascalu. "GLOBAL SENSITIVITY ANALYSIS APPLIED TO A CANCER IMMUNOTHERAPY MODEL." In eLSE 2019. Carol I National Defence University Publishing House, 2019. http://dx.doi.org/10.12753/2066-026x-19-177.
Wang, Haiping, and Ping-Chih Ho. "Abstract A223: CD36-mediated metabolic adaptation guides regulatory T-cells in tumors." In Abstracts: Fourth CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 30 - October 3, 2018; New York, NY. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr18-a223.
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