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Relevant bibliographies by topics / Cell transdifferentiation

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Academic literature on the topic 'Cell transdifferentiation'

Author: Grafiati

Published: 4 June 2021

Last updated: 5 February 2022

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Journal articles on the topic "Cell transdifferentiation"

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OKADA, T. S. "Transdifferentiation in Animal Cells: Fact or Artifact?. (cell commitment/transdifferentiation/cell type conversion)." Development, Growth and Differentiation 28, no. 3 (May 1986): 213–21. http://dx.doi.org/10.1111/j.1440-169x.1986.00213.x.

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Zhao, Zhiliang, Mengyao Xu, Meng Wu, Xiaocheng Tian, Cuiping Zhang, and Xiaobing Fu. "Transdifferentiation of Fibroblasts by Defined Factors." Cellular Reprogramming 17, no. 3 (June 2015): 151–59. http://dx.doi.org/10.1089/cell.2014.0089.

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Maclean, Norman. "Transdifferentiation: Flexibility in cell differentiation." Trends in Biochemical Sciences 17, no. 8 (August 1992): 322. http://dx.doi.org/10.1016/0968-0004(92)90447-h.

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Mitashov, V. I. "Genetic Mechanisms of Cell Transdifferentiation." Russian Journal of Developmental Biology 36, no. 4 (July 2005): 240–46. http://dx.doi.org/10.1007/s11174-005-0039-1.

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Lee, Tsong-Hai, Pei-Shan Liu, Su-Jane Wang, Ming-Ming Tsai, Velayuthaprabhu Shanmugam, and Hsi-Lung Hsieh. "Bradykinin, as a Reprogramming Factor, Induces Transdifferentiation of Brain Astrocytes into Neuron-like Cells." Biomedicines 9, no. 8 (July 30, 2021): 923. http://dx.doi.org/10.3390/biomedicines9080923.

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Kinins are endogenous, biologically active peptides released into the plasma and tissues via the kallikrein-kinin system in several pathophysiological events. Among kinins, bradykinin (BK) is widely distributed in the periphery and brain. Several studies on the neuro-modulatory actions of BK by the B2BK receptor (B2BKR) indicate that this neuropeptide also functions during neural fate determination. Previously, BK has been shown to induce differentiation of nerve-related stem cells into neuron cells, but the response in mature brain astrocytes is unknown. Herein, we used rat brain astrocyte (RBA) to investigate the effect of BK on cell transdifferentiation into a neuron-like cell morphology. Moreover, the signaling mechanisms were explored by zymographic, RT-PCR, Western blot, and immunofluorescence staining analyses. We first observed that BK induced RBA transdifferentiation into neuron-like cells. Subsequently, we demonstrated that BK-induced RBA transdifferentiation is mediated through B2BKR, PKC-δ, ERK1/2, and MMP-9. Finally, we found that BK downregulated the astrocytic marker glial fibrillary acidic protein (GFAP) and upregulated the neuronal marker neuron-specific enolase (NSE) via the B2BKR/PKC-δ/ERK pathway in the event. Therefore, BK may be a reprogramming factor promoting brain astrocytic transdifferentiation into a neuron-like cell, including downregulation of GFAP and upregulation of NSE and MMP-9 via the B2BKR/PKC-δ/ERK cascade. Here, we also confirmed the transdifferentiative event by observing the upregulated neuronal nuclear protein (NeuN). However, the electrophysiological properties of the cells after BK treatment should be investigated in the future to confirm their phenotype.

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English, Denis. "Transdifferentiation Wars." Stem Cells and Development 14, no. 6 (December 2005): 605–7. http://dx.doi.org/10.1089/scd.2005.14.605.

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Eisenberg, Leonard M., and Carol A. Eisenberg. "Stem cell plasticity, cell fusion, and transdifferentiation." Birth Defects Research Part C: Embryo Today: Reviews 69, no. 3 (August 2003): 209–18. http://dx.doi.org/10.1002/bdrc.10017.

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Luo, Liang, Da-Hai Hu, James Q. Yin, and Ru-Xiang Xu. "Molecular Mechanisms of Transdifferentiation of Adipose-Derived Stem Cells into Neural Cells: Current Status and Perspectives." Stem Cells International 2018 (September 13, 2018): 1–14. http://dx.doi.org/10.1155/2018/5630802.

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Neurological diseases can severely compromise both physical and psychological health. Recently, adult mesenchymal stem cell- (MSC-) based cell transplantation has become a potential therapeutic strategy. However, most studies related to the transdifferentiation of MSCs into neural cells have had disappointing outcomes. Better understanding of the mechanisms underlying MSC transdifferentiation is necessary to make adult stem cells more applicable to treating neurological diseases. Several studies have focused on adipose-derived stromal/stem cell (ADSC) transdifferentiation. The purpose of this review is to outline the molecular characterization of ADSCs, to describe the methods for inducing ADSC transdifferentiation, and to examine factors influencing transdifferentiation, including transcription factors, epigenetics, and signaling pathways. Exploring and understanding the mechanisms are a precondition for developing and applying novel cell therapies.

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Huang, Shian, Xiulong Zhu, Wenjun Huang, Yuan He, Lingpin Pang, Xiaozhong Lan, Xiaorong Shui, Yanfang Chen, Can Chen, and Wei Lei. "Quercetin Inhibits Pulmonary Arterial Endothelial Cell Transdifferentiation Possibly by Akt and Erk1/2 Pathways." BioMed Research International 2017 (2017): 1–8. http://dx.doi.org/10.1155/2017/6147294.

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This study aimed to investigate the effects and mechanisms of quercetin on pulmonary arterial endothelial cell (PAEC) transdifferentiation into smooth muscle-like cells. TGF-β1-induced PAEC transdifferentiation models were applied to evaluate the pharmacological actions of quercetin. PAEC proliferation was detected with CCK8 method and BurdU immunocytochemistry. Meanwhile, the identification and transdifferentiation of PAECs were determined by FVIII immunofluorescence staining andα-SMA protein expression. The related mechanism was elucidated based on the levels of Akt and Erk1/2 signal pathways. As a result, quercetin effectively inhibited the TGF-β1-induced proliferation and transdifferentiation of the PAECs and activation of Akt/Erk1/2 cascade in the cells. In conclusion, quercetin is demonstrated to be effective for pulmonary arterial hypertension (PAH) probably by inhibiting endothelial transdifferentiation possibly via modulating Akt and Erk1/2 expressions.

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Corbett, James L., and David Tosh. "Conversion of one cell type into another: implications for understanding organ development, pathogenesis of cancer and generating cells for therapy." Biochemical Society Transactions 42, no. 3 (May 22, 2014): 609–16. http://dx.doi.org/10.1042/bst20140058.

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Metaplasia is the irreversible conversion of one differentiated cell or tissue type into another. Metaplasia usually occurs in tissues that undergo regeneration, and may, in a pathological context, predispose to an increased risk of disease. Studying the conditions leading to the development of metaplasia is therefore of significant clinical interest. In contrast, transdifferentiation (or cellular reprogramming) is a subset of metaplasia that describes the permanent conversion of one differentiated cell type into another, and generally occurs between cells that arise from neighbouring regions of the same germ layer. Transdifferentiation, although rare, has been shown to occur in Nature. New insights into the signalling pathways involved in normal tissue development may be obtained by investigating the cellular and molecular mechanisms in metaplasia and transdifferentiation, and additional identification of key molecular regulators in transdifferentiation and metaplasia could provide new targets for therapeutic treatment of diseases such as cancer, as well as generating cells for transplantation into patients with degenerative disorders. In the present review, we focus on the transdifferentiation of pancreatic cells into hepatocyte-like cells, the development of Barrett's metaplasia in the oesophagus, and the cellular and molecular mechanisms underlying both processes.

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Dissertations / Theses on the topic "Cell transdifferentiation"

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Cambuli, Francesco. "Comparative analysis of ES cell transdifferentiation to TS-like cells." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648815.

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Yuan, Songyang. "Differentiation and transdifferentiation of adult pancreatic cells." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ30425.pdf.

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Madhavan, Mayur C. "Mechanisms of Transdifferentiation and Regeneration." Miami University / OhioLINK, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=miami1133554812.

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Fakhry, Maya. "Molecular mechanisms of vascular smooth muscle cell transdifferentiation into osteochondrocyte-like cells." Thesis, Lyon 1, 2015. http://www.theses.fr/2015LYO10246.

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Chez les patients souffrant d'insuffisance rénale chronique, les calcifications vasculaires représentent la première cause de mortalité. Elles résultent de la trans-différenciation des cellules musculaires lisses (CMLs) en cellules de type ostéoblastique et/ou chondrocytaire, en réponse à des cytokines inflammatoires ou à une hyperphosphatémie. Les CMLs forment alors des cristaux par l'activité de la phosphatase alcaline non-spécifique du tissu (TNAP). A la lumière de résultats récents, nous avons émis l'hypothèse que la TNAP module la trans différenciation des CMLs. Nos objectifs étaient donc de déterminer l'effet de la TNAP dans la trans-différenciation des CMLs, et d'étudier les mécanismes impliqués dans son induction, avec un intérêt particulier pour les microRNAs. Nous avons observé que l'ajout de phosphatase alcaline purifiée ou la surexpression de TNAP stimule l'expression de marqueurs chondrocytaires en culture de CMLs et de cellules souches mésenchymateuses. De plus, l'inhibition de la TNAP bloque la maturation de chondrocytes primaires. Nous excluons un rôle des cristaux formés par la TNAP, puisque l'ajout de cristaux seuls ou associés à une matrice collagénique n'a pas reproduit les effets de la TNAP. Nous suspectons que la TNAP agit en hydrolysant le pyrophosphate inorganique (PPi). En effet, c'est la TNAP qui hydrolyse le PPi en culture de CMLs et de chondrocytes, et le PPi mime les effets de l'inhibition de TNAP en culture de chondrocytes. Enfin, nous rapportons le profil de microRNA des artères cultivées en conditions hyperphosphatémiques. Ces résultats pourraient être particulièrement importants dans le développement de nouvelles approches thérapeutiques
In patients with chronic kidney disease (CKD), vascular calcification represents the main cause of mortality. Vascular calcification results from the trans-differentiation of vascular smooth muscle cells (VSMCs) into cells similar to osteoblasts and/or chondrocytes, in response to inflammatory cytokines or hyperphosphatemia. Calcifying VSMCs form calcium phosphate crystals through the activity of tissue nonspecific alkaline phosphatase (TNAP). In light of recent findings, we hypothesized that TNAP also modulates VSMC trans-differentiation. Our objectives were therefore to determine the effect of TNAP activity on VSMC trans-differentiation, and secondly to investigate the molecular mechanisms involved in TNAP expression in aortas, with a particular interest in microRNAs. We first observed that addition of purified alkaline phosphatase or TNAP over-expression stimulates the expression of chondrocyte markers in culture of the mouse and rat VSMC lines, and of mesenchymal stem cells. Moreover, TNAP inhibition blocks the maturation of mouse primary chondrocytes and reduces mineralization. We exclude a role for crystals in TNAP effects, since addition of crystals alone or associated to a collagenous matrix fails to mimic TNAP effects. We rather suspect that TNAP acts through the hydrolysis of inorganic pyrophosphate (PPi). Indeed, PPi is hydrolyzed by TNAP in VSMCs and chondrocytes and addition of PPi mimics the effects of TNAP inhibition on chondrocyte maturation. Finally, we report microRNA signature of aortic explants treated under hyperphosphatemic conditions that induce vascular calcification. These results could be of particular importance in patients with CKD

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Mojica, Jorge Ricardo. "Commitment and transdifferentiation of adult progenitor cells: The contributing pathways." Thesis, University of Ottawa (Canada), 2008. http://hdl.handle.net/10393/27717.

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C2C12 murine progenitors are a model for transdifferentiation. This project investigated signaling events that regulate this process in culture by monitoring specific markers for transdifferentiation (alkaline phosphatase [ALP] and myogenin for the osteoblastic and myoblaststic fates respectively) in the presence of inducers and inhibitors. Antibodies specific for proteins implicated in signaling were used to monitor the differentiation process. BMP-2 addition caused transdifferentiation to the osteoblastic fate except for a small fraction of cells that may represent the so-called MyoD negative cells or the side population (SP). The timing of short term commitment of C2C12 to osteoblastic transdifferentiation was between 6 to 24h under our culture conditions. BMP-2-induced ALP activity increase and the repression of myogenin expression were not simultaneous. Differentiation as measured by ALP activity may be dependent on the interaction of BMP-2/Smad, p38 MAPK and TGF-beta1 pathways. Smads 1, 5 and/or 8 were almost always found under their phosphorylated form (pSmads) and thus almost invariably located in nuclei suggesting fast nucleoplasmic shuttling from the cytoplasm and nuclear retention of the phosphorylated forms. Phosphorylated forms were also found in the nucleus under proliferative conditions without exogenous BMP-2. In this case, it is suggested that this phosphorylation of Smads may be triggered by the reported autocrine secretion of TGF-beta by the C2C12 cells or by the TGF-beta present in the culture serum.

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Yuan, Yuan. "Small-Molecule Modulators of Pancreatic Ductal Cells: Histone Methyltransferases and \(\beta\)-Cell Transdifferentiation." Thesis, Harvard University, 2012. http://dissertations.umi.com/gsas.harvard:10637.

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Small molecules are important not only for treating human diseases but also for studying disease-related biological processes. This dissertation focuses on the effects of small molecules on pancreatic ductal adenocarcinoma cells. Here, I describe the discovery of two small-molecule tool compounds and their applications for interrogating the biological processes related to two distinct diseases in the human pancreas. First, BRD4770 was identified as a histone methyltransferase inhibitor through a target-based biochemical approach, and was used as a probe to study the function of methyltransferases in cancer cells. Second, BRD7552 was discovered as an inducer of Pdx1 using a cell-based phenotypic screening approach, and was used to induce the expression of Pdx1, a master regulatory transcription factor required for \(\beta\)-cell transdifferentiation. This compound is particularly interesting for the study of type-1 diabetes (T1D). The histone methyltransferase G9a catalyzes methylation of lysine 9 on histone H3, a modification linked to aberrant silencing of tumor-suppressor genes. The second chapter describes the collaborative effort leading to the identification of BRD4770 as a probe to study the function of G9a in human pancreatic cancer cells. BRD4770 induces cellular senescence and inhibits both anchorage-dependent and -independent proliferation in PANC-1 cell line, presumably mediated through ATM-pathway activation. Chapter three describes the study of a natural product gossypol, which significantly enhances the BRD4770 cytotoxicity in p53-mutant cells through autophagic cell death. The up-regulation of BNIP3 might be responsible for the synergistic cell death, suggesting that G9a inhibition may help overcome drug resistance in certain cancer cells. Ectopic overexpression of Pdx1, Ngn3, and MafA can reprogram pancreatic exocrine cells to insulin-producing cells in mice, which sheds light on a new avenue for treating T1D. The fourth chapter focuses on a gene expression-based assay using quantitative real-time PCR technique to screen >60,000 compounds for induction of one or more of these three transcription factors. A novel compound BRD7552 which up-regulated Pdx1 mRNA and protein levels in PANC-1 cells was identified. BRD7552 induces changes of the epigenetic markers within the Pdx1 promoter region consistent with transcriptional activation. Furthermore, BRD7552 partially complements Pdx1 in cell culture, enhancing the expression of insulin induced by the introduction of the three genes in PANC-1 cells. In summary, the central theme of my dissertation is to identify novel bioactive small molecules using different screening approaches, as well as to explore their effects in pancreatic ductal cells.
Chemistry and Chemical Biology

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Barbosa-Sabanero, Karla Y. "Dedifferentiation and transdifferentiation: a study of the RPE cell identity." Miami University / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=miami1468660645.

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Gsour, Amna. "Differentiation of human cell line towards a pancreatic endocrine lineage." Thesis, University of Manchester, 2016. https://www.research.manchester.ac.uk/portal/en/theses/differentiation-of-human-cell-line-towards-a-pancreatic-endocrine-lineage(0c2c21fe-724d-449f-804c-02741c89828c).html.

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Islet transplantations have been successful in restoring glucose homeostasis in patients with diabetes; however, the limited number of donor organs limits the success of this treatment. The lineage reprograming of different cell sources to beta cells potentially provides an unlimited supply of insulin-producing cells for regenerative therapy for patients with diabetes. The aim of this study was to investigate the ability to transdifferentiate two cell lines into an endocrine lineage. Insulin production in pancreatic beta cells can be increased using a small molecule, 3,5-disubstituted isoxazole, N-cyclopropyl-t-(thiophen-2-yl)isoxazole-3-carboxamide (isoxazole) but its effect on other cell types has not been reported. Here, we investigated the lineage reprogramming of PANC-1 pancreatic ductal cells to insulin producing cells by isoxazole treatment. Gene expression was performed using RT-PCR and qPCR for approximately 30 genes critical to beta cell development and function. In addition, quantitative proteomic profiling was performed using LC-MS by monitoring protein abundance in isoxazole-treated PANC-1 cells compared to time-matched controls. Isoxazole treatment stimulated PANC-1 cells to aggregate into islet-like clusters and gene expression analysis revealed induction of important developmental beta cell markers including NGN3, NEUROD1 and INSULIN. In addition, beta cell surface markers were also upregulated such as CD200, GPR50, TROP-2, GLUT2 and SLC30A8. Using LC-MS a catalogue of approximately 2400 identified proteins was generated; 257 proteins were differentially expressed in isoxazole-treated cells compared to DMSO-vehicle controls at p < 0.05. Amongst the proteins upregulated were molecules that regulate metabolic processes and cytoskeletal reorganisation. The expression of the majority of these proteins has not been previously reported or studied in the context of beta cell differentiation. Functional analysis of the relative protein changes was determined using Ingenuity Pathway Analysis, IPA, and gene ontology, GO, software, which revealed the regulation of several cellular canonical pathways including metabolic pathways, cell adhesion, remodelling of epithelial adherens junctions and actin cytoskeleton signalling. The effects of isoxazole were further studied in the A549 lung cancer cell line. Similar effects were observed, such as the induction of pro-endocrine markers NGN3 and NEUROD1 and endocrine-specific hormones INS and GCG. These results indicate that isoxazole has the capacity to transdifferentiate pancreatic and non-pancreatic cell origins into an endocrine lineage. This study reveals the powerful induction capacity of isoxazole in inducing cellular reprogramming events.

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Rapino, Francesca 1982. "Induced transdifferentiation of human B-leukemia/lymphoma cell lines and inhibition of leukemogenicity." Doctoral thesis, Universitat Pompeu Fabra, 2013. http://hdl.handle.net/10803/128575.

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B-cell malignancies encompass a wide variety of distinct diseases including Non Hodgkin lymphoma (NHL) and leukemia. Currently, chemotherapy, radiation and anti-CD20 antibody treatment are the mainstays of B-cell lymphoma and leukemia therapy. However, the fact that a large number of patients are eventually not cured justifies the search for novel and more effective therapeutic approaches. Although induction of differentiation has been shown to be effective in several tumors such as acute promyelocytic leukemia, it has not been tested yet in NHL and leukemia. We therefore hypothesized that transdifferentiation of malignant B cells could be proposed as a novel therapeutic approach. Earlier work of our laboratory demonstrated that the transcription factor C/EBPα could convert immature and mature murine B lineage cells into functional macrophages at high efficiencies. Here we show that the ectopic expression of C/EBPα can likewise induce the conversion of selected human lymphoma and leukemia B-cell lines into macrophages. The reprogrammed cells are functional and quiescent. Importantly, the tumorigenicity of transdifferentiated lymphoma and leukemia cell lines was impaired after transplantation into immunodeficient mice, even when C/EBPα was activated in vivo. In summary, our experiments show for the first time that human cancer cells can be induced to transdifferentiate by C/EBPα into seemingly normal cells at high frequencies, thus proposing transdifferentiation as novel therapeutic approach. In line with this, we believe that the finding of a small molecule that mimics C/EBPα overexpression will open new horizons for the cure of patients affected by B cell malignancies.
Las neoplasias malignas de células B abarcan una amplia variedad de enfermedades diferentes, incluyendo el linfoma no Hodgkin (LNH) y leucemia. Actualmente, la quimioterapia, la radiación y el tratamiento con anticuerpos anti-CD20 son los pilares de la terapia contra el linfoma y la leucemia de células B. Sin embargo, el hecho de que un gran porcentaje de pacientes no se cura con estos tratamientos, justifica la búsqueda de nuevas terapias más eficaces. Aunque la inducción de la diferenciación ha demostrado ser eficaz en el tratamiento de varios tumores tales como la leucemia promielocítica aguda, esta técnica no se ha probado aún en el tratamiento del LNH o de la leucemia. Por lo tanto, la transdiferenciación de las células B malignas podría ser propuesta como un nuevo enfoque terapéutico. Trabajos anteriores de nuestro laboratorio han demostrado que el factor de transcripción C/EBPα puede convertir células de linaje B murinas inmaduras y maduras en macrófagos funcionales con una alta eficiencia. En este trabajo mostramos que la expresión ectópica de C/EBPα puede inducir la conversión de ciertas líneas de linfoma y leucemia humana en macrófagos. Las células reprogramadas son funcionales y quiescientes. Es importante destacar que la tumorigenicidad de linfoma transdiferenciados y líneas celulares de leucemia se vio afectada después del trasplante en ratones inmunodeficientes, incluso cuando C/EBPα se activó in vivo. En resumen, nuestros experimentos muestran por primera vez que las células de cáncer humano pueden ser inducidas por C/EBPα a transdifferenciarse en células aparentemente normales con una alta frecuencia, proponiendo así la transdiferenciación como nuevo enfoque terapéutico. En línea con esto, creemos que el hallazgo de una pequeña molécula que sea capaz de imitar la sobreexpresión de C/EBPα abrirá nuevos horizontes para la cura de los pacientes afectados por tumores malignos de células B.

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Gharibi, Borzo. "Adenosine receptor expression and function during mesenchymal stem cell differentiation and osteoblast transdifferentiation." Thesis, Cardiff University, 2010. http://orca.cf.ac.uk/54352/.

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The mechanisms involved in osteoblast and adipocyte differentiation from the common progenitor, mesenchymal stem cell (MSC) are not fully understood. The nucleoside, adenosine, exists in all cells and is known to be involved in cell growth, proliferation and apoptosis by interacting with four distinct receptors (Ai, A2A, A2b and A3). The aims of this study was to investigate the expression and function of adenosine receptors in 1) MSCs and as they differentiated into osteoblasts and adipocytes and in 2) mouse 7F2 and human osteoblasts and during their transdifferentiation to adipocytes. Rat MSCs and 7F2 osteoblasts expressed all four adenosine receptors. Osteoblast differentiation was associated with increases in A2A and A2B receptor expression and their activation stimulated the expression of alkaline phosphatase, core binding factor a1 and mineralisation. Adenosine also stimulated adipogenesis (lipid accumulation, peroxisome proliferator-activated receptor, CCAAT/enhancer binding protein a and lipoprotein lipase expression) of MSCs which was accompanied by increased A1 and A2A receptor expression. Transdifferentiation of 7F2 cells to adipocytes was associated with increased Ai, but decreased A2A and A2b receptor expression. Loss of A2 receptors in adipocytes was supported by reduced cAMP and extracellular signal regulated kinase responses to adenosine. Adenosine also stimulated transdifferentiation of human osteoblasts to adipocytes by inducing lipoprotein lipase and inhibiting alkaline phosphatase and osteocalcin expression. Overexpression of Ai receptors in 7F2 cells stimulated adipogenesis (lipid accumulation and lipoprotein lipase expression) whereas overexpression of A2b receptors stimulated alkaline phophatase expression and inhibited adipogenesis. These results show that adenosine receptor expression and function is involved in lineage specific differentiation or transdifferentiation A2B receptors are associated with MSCs and osteoblasts and Ai receptors with adipocytes. Targeting adenosine signal pathways may thus be useful as an adjunct therapy for the prevention or treatment of conditions in which there is insufficient bone or excessive adipocyte formation.

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Books on the topic "Cell transdifferentiation"

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Transdifferentiation: Flexibility in cell differentiation. Oxford: Clarendon Press, 1991.

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Book chapters on the topic "Cell transdifferentiation"

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Opas, M. "Cytomechanics of Transdifferentiation." In Cell Mechanics and Cellular Engineering, 233–52. New York, NY: Springer New York, 1994. http://dx.doi.org/10.1007/978-1-4613-8425-0_14.

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Eguchi, Goro. "‘Transdifferentiation’ of Vertebrate Cells in Cell Culture." In Ciba Foundation Symposium 40 - Embryogenesis in Mammals, 241–58. Chichester, UK: John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470720226.ch12.

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Adamska, Maja. "Differentiation and Transdifferentiation of Sponge Cells." In Results and Problems in Cell Differentiation, 229–53. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-92486-1_12.

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McDevitt, David S. "Transdifferentiation in Animals A Model for Differentiation Control." In Genomic Adaptability in Somatic Cell Specialization, 149–73. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4615-6820-9_7.

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Sanges*, Daniela, Frederic Lluis*, and Maria Pia Cosma. "Cell-Fusion-Mediated Reprogramming: Pluripotency or Transdifferentiation? Implications for Regenerative Medicine." In Advances in Experimental Medicine and Biology, 137–59. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-0763-4_9.

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Meivar-Levy, Irit, Hila Barash, and Sarah Ferber. "Transdifferentiation of Extra-Pancreatic Tissues for Cell Replacement Therapy for Diabetes." In Pancreatic Islet Biology, 193–215. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-45307-1_8.

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Xiao, Xinhua, and Yijing Liu. "Cell Transplantation Therapy for Diabetes Mellitus: From Embryonic Stem Cells to Transdifferentiation of Adult Cells." In Translational Medicine Research, 499–510. Dordrecht: Springer Netherlands, 2015. http://dx.doi.org/10.1007/978-94-017-7273-0_21.

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Ries, Christian, and Virginia Egea. "Human Mesenchymal Stem Cell Transdifferentiation to Neural Cells: Role of Tumor Necrosis Factor Alpha." In Stem Cells and Cancer Stem Cells, Volume 8, 71–78. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-4798-2_7.

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Louis, Lithin K., A. Ashwini, Anujith Kumar, and Rajarshi Pal. "Transdifferentiation: A Lineage Instructive Approach Bypassing Roadways of Induced Pluripotent Stem Cell (iPSC)." In Regenerative Medicine: Laboratory to Clinic, 123–42. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-3701-6_8.

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Domínguez-Bendala, Juan. "Transdifferentiation." In Pancreatic Stem Cells, 91–97. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-132-5_7.

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Conference papers on the topic "Cell transdifferentiation"

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Muthukrishnan, SD, M. Johnson, and H. Kornblum. "29 Radiation promotes transdifferentiation of glioblastoma stem cells into vascular cell types." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.29.

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Gopal, Priyanka, Kevin Rogacki, Craig D. Peacock, and Mohamed E. Abazeed. "Abstract 2897: Dynamic transdifferentiation programs in small cell lung carcinoma." 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.am2019-2897.

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Gopal, Priyanka, Kevin Rogacki, Craig D. Peacock, and Mohamed E. Abazeed. "Abstract 2897: Dynamic transdifferentiation programs in small cell lung carcinoma." 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.sabcs18-2897.

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Takeuchi, Kenneth K., Kathleen E. Delgiorno, Christopher J. Halbrook, and Howard C. Crawford. "Abstract IA13: Acinar cell transdifferentiation sets the stage for early tumor heterogeneity." In Abstracts: AACR Special Conference on Pancreatic Cancer: Innovations in Research and Treatment; May 18-21, 2014; New Orleans, LA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.panca2014-ia13.

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Shao, Rong, Steve Scully, Ralph Francescone, Michael Faibish, Brooke Bentley, Sherry L. Taylor, Dennis Oh, Robert Schapiro, Luis Moral, and Wei Yan. "Abstract 1024: Mural cell transdifferentiation of glioblastoma stem-like cells drives vasculogenic mimicry in glioblastoma development." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-1024.

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Volk-Draper, Lisa, Kelly Hall, Michael Flister, and Sophia Ran. "Abstract 400: A new model for macrophage transdifferentiation into lymphatic endothelial cell progenitors." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-400.

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"The first insights into regulation of cell transdifferentiation during gut regeneration in Eupentacta fraudatrix." In Bioinformatics of Genome Regulation and Structure/ Systems Biology. institute of cytology and genetics siberian branch of the russian academy of science, Novosibirsk State University, 2020. http://dx.doi.org/10.18699/bgrs/sb-2020-005.

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Zhou, Beiyun, Yixin Liu, Crystal Marconett, David K. Ann, Per Flodby, Parviz Minoo, Michael Kahn, Edward D. Crandall, Ite A. Laird-Offringa, and Zea Borok. "HDAC3 And GATA-6/p300 Coordinately Regulate Type I Cell-Specific Aquaporin-5 (Aqp5) Gene Expression During Alveolar Epithelial Cell (AEC) Transdifferentiation." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4217.

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Réthi, B., A. Krishnamurthy, J. Ytterberg, M. Sun, V. Joshua, H. Wähämaa, N. Tarasova, J. Steen, V. Malmström, and AI Catrina. "FRI0006 Protein citrullinations by pad enzymes promote dendritic cell transdifferentiation into osteoclast and generate targets for ra-specific antibodies." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.5971.

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Togo, Shinsaku, Kumi Nagahama, Xiangde Liu, Yoko Gunji, Kazuya Takamochi, Kenji Suzuki, Stephen I. Rennard, and Kazuhisa Takahashi. "Stromal Fibroblasts Associated With Lung Cancer Cells Enhanced Transdifferentiation Into Myofibroblast." 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.a5555.

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Reports on the topic "Cell transdifferentiation"

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Du, Cheng. Transdifferentiation between Luminal- and Basal-Type Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, December 2013. http://dx.doi.org/10.21236/ada601036.

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