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Journal articles on the topic 'Cell differentiation'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

Zhang, Yu, Patrick Babczyk, Andreas Pansky, Matthias Ulrich Kassack, and Edda Tobiasch. "P2 Receptors Influence hMSCs Differentiation towards Endothelial Cell and Smooth Muscle Cell Lineages." International Journal of Molecular Sciences 21, no. 17 (2020): 6210. http://dx.doi.org/10.3390/ijms21176210.

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Background: Human mesenchymal stem cells (hMSCs) have shown their multipotential including differentiating towards endothelial and smooth muscle cell lineages, which triggers a new interest for using hMSCs as a putative source for cardiovascular regenerative medicine. Our recent publication has shown for the first time that purinergic 2 receptors are key players during hMSC differentiation towards adipocytes and osteoblasts. Purinergic 2 receptors play an important role in cardiovascular function when they bind to extracellular nucleotides. In this study, the possible functional role of purine

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2

J, Otsuka. "A Theoretical Study on the Cell Differentiation Forming Stem Cells in Higher Animals." Physical Science & Biophysics Journal 5, no. 2 (2021): 1–10. http://dx.doi.org/10.23880/psbj-16000191.

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The recent genome sequencing of multicellular diploid eukaryotes reveals an enlarged repertoire of protein genes for signal transmission but it is still difficult to elucidate the network of signal transmission to drive the life cycle of such an eukaryote only from biochemical and genetic studies. In the present paper, a theoretical study is carried out for the cell differentiation, the formation of stem cells and the growth from a child to the adult in the higher animal. With the intercellular and intracellular signal transmission in mind, the cell differentiation is theoretically derived fro

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3

Fuchs, Elaine, and Eric Olson. "Cell differentiation." Current Opinion in Cell Biology 8, no. 6 (1996): 823–25. http://dx.doi.org/10.1016/s0955-0674(96)80083-4.

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4

Fuchs, Elaine, and Fiona M. Watt. "Cell differentiation." Current Opinion in Cell Biology 15, no. 6 (2003): 738–39. http://dx.doi.org/10.1016/j.ceb.2003.10.018.

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5

Goldstein, Lawrence, and Sean Morrison. "Cell differentiation." Current Opinion in Cell Biology 16, no. 6 (2004): 679–80. http://dx.doi.org/10.1016/j.ceb.2004.10.001.

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6

Brand, Andrea H., and Frederick J. Livesey. "Cell differentiation." Current Opinion in Cell Biology 17, no. 6 (2005): 637–38. http://dx.doi.org/10.1016/j.ceb.2005.10.007.

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7

Bronner-Fraser, Marianne. "Cell differentiation." Current Opinion in Cell Biology 18, no. 6 (2006): 690–91. http://dx.doi.org/10.1016/j.ceb.2006.10.011.

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8

Farmer, Stephen R., and Bruce M. Spiegelman. "Cell differentiation." Current Opinion in Cell Biology 19, no. 6 (2007): 603–4. http://dx.doi.org/10.1016/j.ceb.2007.11.002.

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9

Derynck, Rik, and ErwinF Wagner. "Cell differentiation." Current Opinion in Cell Biology 7, no. 6 (1995): 843–44. http://dx.doi.org/10.1016/0955-0674(95)80068-9.

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10

Steel, Michael. "CELL DIFFERENTIATION." Lancet 341, no. 8854 (1993): 1187–88. http://dx.doi.org/10.1016/0140-6736(93)91010-j.

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11

Lindholm, Dan, and Urmas Arumäe. "Cell differentiation." Journal of Cell Biology 167, no. 2 (2004): 193–95. http://dx.doi.org/10.1083/jcb.200409171.

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The molecular mechanisms by which differentiated cells combat cell death and injury have remained unclear. In the current issue, it has been shown in neurons that cell differentiation is accompanied by a decrease in Apaf-1 and the activity of the apoptosome with an increased ability of the inhibitor of apoptosis proteins (IAPs) to sustain survival (Wright et al., 2004). These results, together with earlier ones, deepen our understanding of how cell death and the apoptosome are regulated during differentiation and in tumor cells.

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12

Bennett, Vann. "Cell differentiation." Current Opinion in Cell Biology 20, no. 6 (2008): 607–8. http://dx.doi.org/10.1016/j.ceb.2008.10.006.

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13

Ogushi, Fumiko, and Hiroshi Kori. "3P277 Dependence of cell differentiation ratio on cell-cell interaction and noise(24. Mathematical biology,Poster)." Seibutsu Butsuri 53, supplement1-2 (2013): S257. http://dx.doi.org/10.2142/biophys.53.s257_6.

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14

Pines, Jonathon, and Frank Lafont. "Cell differentiation and Cell multiplication." Current Opinion in Cell Biology 13, no. 6 (2001): 657–58. http://dx.doi.org/10.1016/s0955-0674(00)00266-0.

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15

Curti, Antonio, Elisa Ferri, Simona Pandolfi, Alessandro Isidori, and Roberto M. Lemoli. "Dendritic Cell Differentiation." Journal of Immunology 172, no. 1 (2003): 3–4. http://dx.doi.org/10.4049/jimmunol.172.1.3.

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16

Salim, Ali, Amato J. Giaccia, and Michael T. Longaker. "Stem cell differentiation." Nature Biotechnology 22, no. 7 (2004): 804–5. http://dx.doi.org/10.1038/nbt0704-804.

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17

James, SharonY, MarcA Williams, AdrianC Newland, and KayW Colston. "Leukemia Cell Differentiation." General Pharmacology: The Vascular System 32, no. 1 (1999): 143–54. http://dx.doi.org/10.1016/s0306-3623(98)00098-6.

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18

Rosenthal, N. "Muscle cell differentiation." Current Opinion in Cell Biology 1, no. 6 (1989): 1094–101. http://dx.doi.org/10.1016/s0955-0674(89)80056-0.

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19

Zorick, Todd S., and Greg Lemke. "Schwann cell differentiation." Current Opinion in Cell Biology 8, no. 6 (1996): 870–76. http://dx.doi.org/10.1016/s0955-0674(96)80090-1.

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20

Sinkovics, Joseph G. "Chondrosarcoma cell differentiation." Pathology & Oncology Research 10, no. 3 (2004): 174–87. http://dx.doi.org/10.1007/bf03033749.

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21

Gusterson, B. "Tumor Cell Differentiation." Journal of Clinical Pathology 41, no. 4 (1988): 480. http://dx.doi.org/10.1136/jcp.41.4.480-c.

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22

MacDonald, H. R. "T-cell differentiation." Research in Immunology 140, no. 5-6 (1989): 635–36. http://dx.doi.org/10.1016/0923-2494(89)90126-0.

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23

Reth, M. "B-cell differentiation." Research in Immunology 140, no. 5-6 (1989): 636–38. http://dx.doi.org/10.1016/0923-2494(89)90127-2.

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24

Lin, Mong-Shang, and Yung-Wu Chen. "B Cell Differentiation." Cellular Immunology 150, no. 2 (1993): 343–52. http://dx.doi.org/10.1006/cimm.1993.1202.

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25

Miller, R. G. "T cell differentiation." International Journal of Cell Cloning 4, S1 (1986): 26–38. http://dx.doi.org/10.1002/stem.5530040708.

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26

Dorshkind, Kenneth. "B-cell differentiation." Immunology Today 7, no. 11 (1986): 322–23. http://dx.doi.org/10.1016/0167-5699(86)90131-3.

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27

Xu, Wei, Chirag H. Patel, Jesse Alt, et al. "GOT1 constrains TH17 cell differentiation, while promoting iTreg cell differentiation." Nature 614, no. 7946 (2023): E1—E11. http://dx.doi.org/10.1038/s41586-022-05602-3.

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28

Vaidya, Milind M., and Deepak Kanojia. "Keratins: Markers of cell differentiation or regulators of cell differentiation?" Journal of Biosciences 32, no. 4 (2007): 629–34. http://dx.doi.org/10.1007/s12038-007-0062-8.

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29

Clark, Allison J., Kathryn M. Doyle, and Patrick O. Humbert. "Cell-intrinsic requirement for pRb in erythropoiesis." Blood 104, no. 5 (2004): 1324–26. http://dx.doi.org/10.1182/blood-2004-02-0618.

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Abstract Retinoblastoma (Rb) and family members have been implicated as key regulators of cell proliferation and differentiation. In particular, accumulated data have suggested that the Rb gene product pRb is an important controller of erythroid differentiation. However, current published data are conflicting as to whether the role of pRb in erythroid cells is cell intrinsic or non–cell intrinsic. Here, we have made use of an in vitro erythroid differentiation culture system to determine the cell-intrinsic requirement for pRb in erythroid differentiation. We demonstrate that the loss of pRb fu

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30

Thoma, Eva C., Katja Maurus, Toni U. Wagner, and Manfred Schartl. "Parallel Differentiation of Embryonic Stem Cells into Different Cell Types by a Single Gene-Based Differentiation System." Cellular Reprogramming 14, no. 2 (2012): 106–11. http://dx.doi.org/10.1089/cell.2011.0067.

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31

Valtieri, M., G. Boccoli, U. Testa, C. Barletta, and C. Peschle. "Two-step differentiation of AML-193 leukemic line: terminal maturation is induced by positive interaction of retinoic acid with granulocyte colony-stimulating factor (CSF) and vitamin D3 with monocyte CSF." Blood 77, no. 8 (1991): 1804–12. http://dx.doi.org/10.1182/blood.v77.8.1804.1804.

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Abstract The human AML-193 cell line requires exogenous granulocyte-monocyte colony-stimulating factor (GM-CSF) or interleukin-3 (IL-3) for growth in liquid or semisolid medium. However, these CSFs do not stimulate the differentiation of the cell line. We show that addition of all-trans retinoic acid (RA) or 1,25 dihydroxyvitamin D3 (D3) induces AML-193 cells to differentiate into the granulocytic or monocytic lineage, respectively. On the other hand, addition of either G- or M-CSF alone exerts virtually no differentiative effect. Terminal granulocytic or monocytic differentiation was observed

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32

Valtieri, M., G. Boccoli, U. Testa, C. Barletta, and C. Peschle. "Two-step differentiation of AML-193 leukemic line: terminal maturation is induced by positive interaction of retinoic acid with granulocyte colony-stimulating factor (CSF) and vitamin D3 with monocyte CSF." Blood 77, no. 8 (1991): 1804–12. http://dx.doi.org/10.1182/blood.v77.8.1804.bloodjournal7781804.

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The human AML-193 cell line requires exogenous granulocyte-monocyte colony-stimulating factor (GM-CSF) or interleukin-3 (IL-3) for growth in liquid or semisolid medium. However, these CSFs do not stimulate the differentiation of the cell line. We show that addition of all-trans retinoic acid (RA) or 1,25 dihydroxyvitamin D3 (D3) induces AML-193 cells to differentiate into the granulocytic or monocytic lineage, respectively. On the other hand, addition of either G- or M-CSF alone exerts virtually no differentiative effect. Terminal granulocytic or monocytic differentiation was observed when AML

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33

Filvaroff, E., D. F. Stern, and G. P. Dotto. "Tyrosine phosphorylation is an early and specific event involved in primary keratinocyte differentiation." Molecular and Cellular Biology 10, no. 3 (1990): 1164–73. http://dx.doi.org/10.1128/mcb.10.3.1164-1173.1990.

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Very little is known about early molecular events triggering epithelial cell differentiation. We have examined the possible role of tyrosine phosphorylation in this process, as observed in cultures of primary mouse keratinocytes after exposure to calcium or 12-O-tetradecanoylphorbol-13-acetate (TPA). Immunoblotting with phosphotyrosine-specific antibodies as well as direct phosphoamino acid analysis revealed that induction of tyrosine phosphorylation occurs as a very early and specific event in keratinocyte differentiation. Very little or no induction of tyrosine phosphorylation was observed i

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34

Filvaroff, E., D. F. Stern, and G. P. Dotto. "Tyrosine phosphorylation is an early and specific event involved in primary keratinocyte differentiation." Molecular and Cellular Biology 10, no. 3 (1990): 1164–73. http://dx.doi.org/10.1128/mcb.10.3.1164.

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Very little is known about early molecular events triggering epithelial cell differentiation. We have examined the possible role of tyrosine phosphorylation in this process, as observed in cultures of primary mouse keratinocytes after exposure to calcium or 12-O-tetradecanoylphorbol-13-acetate (TPA). Immunoblotting with phosphotyrosine-specific antibodies as well as direct phosphoamino acid analysis revealed that induction of tyrosine phosphorylation occurs as a very early and specific event in keratinocyte differentiation. Very little or no induction of tyrosine phosphorylation was observed i

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35

Turksen, Kursad, and Tammy-Claire Troy. "Epidermal cell lineage." Biochemistry and Cell Biology 76, no. 6 (1998): 889–98. http://dx.doi.org/10.1139/o98-088.

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The epidermis is a stratified squamous epithelium, which is under a constant state of proliferation, commitment, differentiation, and elimination so that the functional integrity of the tissue is maintained. The intact epidermis has the ability to respond to diverse environmental stimuli by continuous turnover to maintain its normal homeostasis throughout an organism's life. This is achieved by a tightly regulated balance between stem cell self-renewal and the generation of a population of cells that undergo a limited number of more rapid (amplifying) transit divisions before giving rise to no

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36

Matthews, K. R., and K. Gull. "Evidence for an interplay between cell cycle progression and the initiation of differentiation between life cycle forms of African trypanosomes." Journal of Cell Biology 125, no. 5 (1994): 1147–56. http://dx.doi.org/10.1083/jcb.125.5.1147.

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Successful transmission of the African trypanosome between the mammalian host blood-stream and the tsetse fly vector involves dramatic alterations in the parasite's morphology and biochemistry. This differentiation through to the tsetse midgut procyclic form is accompanied by re-entry into a proliferative cell cycle. Using a synchronous differentiation model and a variety of markers diagnostic for progress through both differentiation and the cell cycle, we have investigated the interplay between these two processes. Our results implicate a relationship between the trypanosome cell cycle posit

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37

Park, Hyo Eun, Donghee Kim, Hyun Sook Koh, Sungbo Cho, Jung-Suk Sung, and Jae Young Kim. "Real-Time Monitoring of Neural Differentiation of Human Mesenchymal Stem Cells by Electric Cell-Substrate Impedance Sensing." Journal of Biomedicine and Biotechnology 2011 (2011): 1–8. http://dx.doi.org/10.1155/2011/485173.

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Stem cells are useful for cell replacement therapy. Stem cell differentiation must be monitored thoroughly and precisely prior to transplantation. In this study we evaluated the usefulness of electric cell-substrate impedance sensing (ECIS) forin vitroreal-time monitoring of neural differentiation of human mesenchymal stem cells (hMSCs). We cultured hMSCs in neural differentiation media (NDM) for 6 days and examined the time-course of impedance changes with an ECIS array. We also monitored the expression of markers for neural differentiation, total cell count, and cell cycle profiles. Cellular

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38

Nagayama, Masafumi, Tsutomu Uchida, Toshio Taira, Kyoko Shimizu, Masato Sakai, and Kazutoshi Gohara. "1P460 Cell division of primary stromal-vascular cells during adipose differentiation(21. Development and differentiation,Poster Session,Abstract,Meeting Program of EABS &BSJ 2006)." Seibutsu Butsuri 46, supplement2 (2006): S261. http://dx.doi.org/10.2142/biophys.46.s261_4.

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39

Qiu, Zhijuan, Camille Khairallah, Jessica Nancy Imperato, et al. "Lymph Node Priming Licenses Intestinal CD103+ CD8 Tissue-Resident Memory T Cell Development." Journal of Immunology 204, no. 1_Supplement (2020): 232.8. http://dx.doi.org/10.4049/jimmunol.204.supp.232.8.

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Abstract CD8 tissue-resident memory T (TRM) cells provide front-line protective immunity at barrier tissues. Understanding TRM cell development will provide significant insights for vaccine design targeting infections and cancers at barrier tissues. Here, we demonstrate that pathogen-induced inflammation and pathogen-derived cognate antigen had minimal impact on intestinal CD103+ TRM cell differentiation. Instead, T cell priming in the mesenteric lymph nodes (MLN) was the principal determinant of CD103+ TRM cell differentiation in the intestine. In contrast, T cells primed in the spleen were i

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40

Santos, Mark, Wenying Zhang, Jason Whalley, and Matthew Hsu. "Rapid assessment of CD4 + T cell differentiation towards more specialized cell types using impedance based technology (P6325)." Journal of Immunology 190, no. 1_Supplement (2013): 184.24. http://dx.doi.org/10.4049/jimmunol.190.supp.184.24.

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Abstract Cellular differentiation is a fundamental process in developmental biology. Progenitor cells must have the ability to differentiate into more specialized cell types for the body to respond to infections during autoimmunity. In an immunological response to infections, CD4+ T cells can give rise to a variety of T helper cells depending on the nature of the immune response, and subsequently release a distinct subset of signature cytokines. Similarly, when monocytes are exposed to established lineage specific conditions in vitro, human monocytes differentiate toward mature dendritic cells

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41

Ulmschneider, Bryne, Bree K. Grillo-Hill, Marimar Benitez, Dinara R. Azimova, Diane L. Barber, and Todd G. Nystul. "Increased intracellular pH is necessary for adult epithelial and embryonic stem cell differentiation." Journal of Cell Biology 215, no. 3 (2016): 345–55. http://dx.doi.org/10.1083/jcb.201606042.

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Despite extensive knowledge about the transcriptional regulation of stem cell differentiation, less is known about the role of dynamic cytosolic cues. We report that an increase in intracellular pH (pHi) is necessary for the efficient differentiation of Drosophila adult follicle stem cells (FSCs) and mouse embryonic stem cells (mESCs). We show that pHi increases with differentiation from FSCs to prefollicle cells (pFCs) and follicle cells. Loss of the Drosophila Na+–H+ exchanger DNhe2 lowers pHi in differentiating cells, impairs pFC differentiation, disrupts germarium morphology, and decreases

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42

Andrés, V., and K. Walsh. "Myogenin expression, cell cycle withdrawal, and phenotypic differentiation are temporally separable events that precede cell fusion upon myogenesis." Journal of Cell Biology 132, no. 4 (1996): 657–66. http://dx.doi.org/10.1083/jcb.132.4.657.

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During terminal differentiation of skeletal myoblasts, cells fuse to form postmitotic multinucleated myotubes that cannot reinitiate DNA synthesis. Here we investigated the temporal relationships among these events during in vitro differentiation of C2C12 myoblasts. Cells expressing myogenin, a marker for the entry of myoblasts into the differentiation pathway, were detected first during myogenesis, followed by the appearance of mononucleated cells expressing both myogenin and the cell cycle inhibitor p21. Although expression of both proteins was sustained in mitogen-restimulated myocytes, 5-b

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43

Pines, Jonathon, Luca Toldo, and Frank Lafont. "Web alert Cell multiplication Cell differentiation." Current Opinion in Cell Biology 9, no. 6 (1997): 755–56. http://dx.doi.org/10.1016/s0955-0674(97)80073-7.

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44

Cohen, Stephen, and Kai Simons. "Cell differentiation Cell asymmetry in development." Current Opinion in Cell Biology 9, no. 6 (1997): 831–32. http://dx.doi.org/10.1016/s0955-0674(97)80084-1.

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45

Pines, Jonathon, Luca Toldo, and Frank Lafont. "Cell differentiation Cell multiplication Web alert." Current Opinion in Cell Biology 10, no. 6 (1998): 683–84. http://dx.doi.org/10.1016/s0955-0674(98)80106-3.

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46

Polonsky, Michal, Jacob Rimer, Amos Kern-Perets, et al. "Induction of CD4 T cell memory by local cellular collectivity." Science 360, no. 6394 (2018): eaaj1853. http://dx.doi.org/10.1126/science.aaj1853.

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Cell differentiation is directed by signals driving progenitors into specialized cell types. This process can involve collective decision-making, when differentiating cells determine their lineage choice by interacting with each other. We used live-cell imaging in microwell arrays to study collective processes affecting differentiation of naïve CD4+ T cells into memory precursors. We found that differentiation of precursor memory T cells sharply increases above a threshold number of locally interacting cells. These homotypic interactions involve the cytokines interleukin-2 (IL-2) and IL-6, whi

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47

Weber, MC, and ML Tykocinski. "Bone marrow stromal cell blockade of human leukemic cell differentiation." Blood 83, no. 8 (1994): 2221–29. http://dx.doi.org/10.1182/blood.v83.8.2221.bloodjournal8382221.

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Bone marrow (BM) stromal cell inhibition of leukemic cell differentiation was studied in cellular coculture experiments. In coculture, a significant percentage of cells from the human myeloid leukemic cell lines HL-60, PLB-985, and K562 adhere to fibroblastic KM- 102 BM stromal cells. A sensitive two-color immunofluorescence assay was developed to monitor stromal cellular effects upon leukemic cell differentiation. After chemical induction with 1 alpha,25- dihydroxyvitamin D3, strongly adherent HL-60 and PLB-985 cells were inhibited from differentiating into more mature monocytic cells, as mea

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48

Qiu, Zhijuan, Camille Khairallah, Timothy H. Chu, et al. "Mesenteric lymph node priming licenses intestinal CD103+ CD8 tissue-resident memory T cell development." Journal of Immunology 206, no. 1_Supplement (2021): 55.02. http://dx.doi.org/10.4049/jimmunol.206.supp.55.02.

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Abstract CD8 tissue-resident memory T (TRM) cells provide front-line protective immunity at barrier tissues; however, mechanisms regulating their development are not completely understood. Priming dictates the migration of effector CD8 T cells to the tissue, while factors in the tissue induce in situ TRM cell differentiation. Whether priming also regulates in situ differentiation of CD8 TRM cells has not been addressed. Here, we demonstrate that T cell priming in the mesenteric lymph nodes (MLN) was the principal determinant of CD103+ CD8 TRM cell differentiation in the intestine. In contrast,

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49

Lees, Simon J., Christopher R. Rathbone, and Frank W. Booth. "Age-associated decrease in muscle precursor cell differentiation." American Journal of Physiology-Cell Physiology 290, no. 2 (2006): C609—C615. http://dx.doi.org/10.1152/ajpcell.00408.2005.

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Muscle precursor cells (MPCs) are required for the regrowth, regeneration, and/or hypertrophy of skeletal muscle, which are deficient in sarcopenia. In the present investigation, we have addressed the issue of age-associated changes in MPC differentiation. MPCs, including satellite cells, were isolated from both young and old rat skeletal muscle with a high degree of myogenic purity (>90% MyoD and desmin positive). MPCs isolated from skeletal muscle of 32-mo-old rats exhibited decreased differentiation into myotubes and demonstrated decreased myosin heavy chain (MHC) and muscle creatine kin

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50

Messina, Graziella, Cristiana Blasi, Severina Anna La Rocca, Monica Pompili, Attilio Calconi, and Milena Grossi. "p27Kip1 Acts Downstream of N-Cadherin-mediated Cell Adhesion to Promote Myogenesis beyond Cell Cycle Regulation." Molecular Biology of the Cell 16, no. 3 (2005): 1469–80. http://dx.doi.org/10.1091/mbc.e04-07-0612.

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It is widely acknowledged that cultured myoblasts can not differentiate at very low density. Here we analyzed the mechanism through which cell density influences myogenic differentiation in vitro. By comparing the behavior of C2C12 myoblasts at opposite cell densities, we found that, when cells are sparse, failure to undergo terminal differentiation is independent from cell cycle control and reflects the lack of p27Kip1 and MyoD in proliferating myoblasts. We show that inhibition of p27Kip1 expression impairs C2C12 cell differentiation at high density, while exogenous p27Kip1 allows low-densit

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