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Journal articles on the topic 'Cellular differentiation'

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Author: Grafiati

Published: 4 June 2021

Last updated: 20 February 2023

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1

Yap, Lynn, Hwee Goon Tay, Mien T. X. Nguyen, Monica S. Tjin, and Karl Tryggvason. "Laminins in Cellular Differentiation." Trends in Cell Biology 29, no. 12 (December 2019): 987–1000. http://dx.doi.org/10.1016/j.tcb.2019.10.001.

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2

Soraisam, Purnabati, G. TempySangma, Th Naranbabu Singh, N. Saratchandra Singh, and M. Shyamo Singh. "Cellular Differentiation of Developing Pancreas in Human Fetuses of Manipuri Origin." Scholars Journal of Applied Medical Sciences 4, no. 7 (July 2016): 2332–37. http://dx.doi.org/10.21276/sjams.2016.4.7.5.

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3

Kretz, Markus. "TINCR, staufen1, and cellular differentiation." RNA Biology 10, no. 10 (October 2013): 1597–601. http://dx.doi.org/10.4161/rna.26249.

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4

Kirsch, Thorsten. "Osteoarthritis: a cellular differentiation defect?" Current Opinion in Orthopaedics 14, no. 5 (October 2003): 356–61. http://dx.doi.org/10.1097/00001433-200310000-00009.

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5

Fusenig, N. E., D. Breitkreutz, H. J. Stark, P. Tomakidi, W. Peter, and P. Boukamp. "Cellular differentiation and tumor progression." Melanoma Research 3 (September 1993): 3. http://dx.doi.org/10.1097/00008390-199309002-00004.

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6

SOHAL, R. S., R. G. ALLEN, and C. NATIONS. "Oxidative Stress and Cellular Differentiation." Annals of the New York Academy of Sciences 551, no. 1 Membrane in C (December 1988): 59–73. http://dx.doi.org/10.1111/j.1749-6632.1988.tb22320.x.

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7

Levine, Joe H., Michelle E. Fontes, Jonathan Dworkin, and Michael B. Elowitz. "Pulsed Feedback Defers Cellular Differentiation." PLoS Biology 10, no. 1 (January 31, 2012): e1001252. http://dx.doi.org/10.1371/journal.pbio.1001252.

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8

Misago, Noriyuki, Toshimi Satoh, and Yutaka Narisawa. "Cellular neurothekeoma with histiocytic differentiation." Journal of Cutaneous Pathology 31, no. 8 (July 22, 2004): 568–72. http://dx.doi.org/10.1111/j.0303-6987.2004.00223.x.

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9

Sager, B., and D. Kaiser. "Spatial restriction of cellular differentiation." Genes & Development 7, no. 9 (September 1, 1993): 1645–53. http://dx.doi.org/10.1101/gad.7.9.1645.

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10

Langdale, Jane A. "Cellular differentiation in the leaf." Current Opinion in Cell Biology 10, no. 6 (December 1998): 734–38. http://dx.doi.org/10.1016/s0955-0674(98)80115-4.

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11

Bulusu, Vinay, and Alexander Aulehla. "Metabolic Control of Cellular Differentiation." Developmental Cell 39, no. 3 (November 2016): 286–87. http://dx.doi.org/10.1016/j.devcel.2016.10.019.

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12

Mohlin, Sofie, Caroline Wigerup, Annika Jögi, and Sven Påhlman. "Hypoxia, pseudohypoxia and cellular differentiation." Experimental Cell Research 356, no. 2 (July 2017): 192–96. http://dx.doi.org/10.1016/j.yexcr.2017.03.007.

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13

Steinberg, Marissa, and Jared Robins. "Cellular Models of Trophoblast Differentiation." Seminars in Reproductive Medicine 34, no. 01 (January 11, 2016): 050–56. http://dx.doi.org/10.1055/s-0035-1570026.

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14

Moyes, C. D., O. A. Mathieu-Costello, N. Tsuchiya, C. Filburn, and R. G. Hansford. "Mitochondrial biogenesis during cellular differentiation." American Journal of Physiology-Cell Physiology 272, no. 4 (April 1, 1997): C1345—C1351. http://dx.doi.org/10.1152/ajpcell.1997.272.4.c1345.

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Mitochondrial biogenesis was studied during differentiation of two immortalized cell lines (C2C12, 3T3) with enzyme measurements, Northern blots, and quantitative ultrastructure. Citrate synthase, isocitrate dehydrogenase, and 3-hydroxyacyl-CoA dehydrogenase (nuclear encoded, mitochondrial matrix location) showed linear, four- to sixfold increases in enzymatic activity in C2C12 cells but increased exponentially in 3T3 cells. Cytochrome oxidase and NADH dehydrogenase (nuclear and mitochondrial encoded, cristae location) increased to a lesser extent and with a pattern dissimilar to the first group. Northern blots and activity of succinate dehydrogenase (cristae location but entirely nuclear encoded) suggested the groupings were based on location of the genes rather than the mature enzyme. However, quantitative electron microscopy and comparisons with adult tissue suggested that mitochondrial ultrastructure can influence the change in cristae enzymes. Cristae surface area per unit mitochondrial volume and per unit cell volume increased much less than did cristae enzymes. Available space on the inner membrane may become limiting and account for some aspects of the pattern of change in electron transport enzymes during differentiation.

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15

Polonsky, Michal, Jacob Rimer, Amos Kern-Perets, Irina Zaretsky, Stav Miller, Chamutal Bornstein, Eyal David, et al. "Induction of CD4 T cell memory by local cellular collectivity." Science 360, no. 6394 (June 14, 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, which affect memory differentiation orthogonal to their effect on proliferation and survival. Mathematical modeling suggests that the differentiation rate is continuously modulated by the instantaneous number of locally interacting cells. This cellular collectivity can prioritize allocation of immune memory to stronger responses.

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16

Kurata, Kosaku, Hidehiko Higaki, and H. Kalervo Vaananen. "Bone Marrow Cell Differentiation Regulated by Gel-embedded Osteocytes(Cellular & Tissue Engineering)." Proceedings of the Asian Pacific Conference on Biomechanics : emerging science and technology in biomechanics 2004.1 (2004): 91–92. http://dx.doi.org/10.1299/jsmeapbio.2004.1.91.

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17

Beauchamp, George R., David Lubeck, and Paul L. Knepper. "Glycoconjugates, Cellular Differentiation, and Congenital Glaucoma." Journal of Pediatric Ophthalmology & Strabismus 22, no. 4 (July 1985): 149–55. http://dx.doi.org/10.3928/0191-3913-19850701-11.

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18

Herrmann, Jennifer C., Robert A. Beagrie, and Jim R. Hughes. "Making connections: enhancers in cellular differentiation." Trends in Genetics 38, no. 4 (April 2022): 395–408. http://dx.doi.org/10.1016/j.tig.2021.10.008.

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19

Zhang, Mingzi M., and Howard C. Hang. "Protein S-palmitoylation in cellular differentiation." Biochemical Society Transactions 45, no. 1 (February 8, 2017): 275–85. http://dx.doi.org/10.1042/bst20160236.

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Reversible protein S-palmitoylation confers spatiotemporal control of protein function by modulating protein stability, trafficking and activity, as well as protein–protein and membrane–protein associations. Enabled by technological advances, global studies revealed S-palmitoylation to be an important and pervasive posttranslational modification in eukaryotes with the potential to coordinate diverse biological processes as cells transition from one state to another. Here, we review the strategies and tools to analyze in vivo protein palmitoylation and interrogate the functions of the enzymes that put on and take off palmitate from proteins. We also highlight palmitoyl proteins and palmitoylation-related enzymes that are associated with cellular differentiation and/or tissue development in yeasts, protozoa, mammals, plants and other model eukaryotes.

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20

Fraser, James, Mathieu Rousseau, Solomon Shenker, Maria A. Ferraiuolo, Yoshihide Hayashizaki, Mathieu Blanchette, and Josée Dostie. "Chromatin conformation signatures of cellular differentiation." Genome Biology 10, no. 4 (2009): R37. http://dx.doi.org/10.1186/gb-2009-10-4-r37.

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21

Chang, Sung-Eun, Tae-Jin Lee, Jae Y. Ro, Jee-Ho Choi, Kyung-Jeh Sung, Kee-Chan Moon, and Jai-Kyoung Koh. "Cellular Neurothekeoma with Possible Neuroendocrine Differentiation." Journal of Dermatology 26, no. 6 (June 1999): 363–67. http://dx.doi.org/10.1111/j.1346-8138.1999.tb03489.x.

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22

Bignami, F., P. Bevilacqua, S. Biagioni, A. De Jaco, F. Casamenti, A. Felsani, and G. Augusti-Tocco. "Cellular Acetylcholine Content and Neuronal Differentiation." Journal of Neurochemistry 69, no. 4 (October 1997): 1374–81. http://dx.doi.org/10.1046/j.1471-4159.1997.69041374.x.

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23

Martin, Cathie, and Beverley J. Glover. "Cellular differentiation in the shoot epidermis." Current Opinion in Plant Biology 1, no. 6 (December 1998): 511–19. http://dx.doi.org/10.1016/s1369-5266(98)80044-7.

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24

Stemple, Derek L., and Wolfgang Driever. "Zebrafish: tools for investigating cellular differentiation." Current Opinion in Cell Biology 8, no. 6 (December 1996): 858–64. http://dx.doi.org/10.1016/s0955-0674(96)80088-3.

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25

Streuli, Charles. "Extracellular matrix remodelling and cellular differentiation." Current Opinion in Cell Biology 11, no. 5 (October 1999): 634–40. http://dx.doi.org/10.1016/s0955-0674(99)00026-5.

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26

Jakt, Lars Martin, Satoko Moriwaki, and Shinichi Nishikawa. "18-P017 Cellular parameterisation of differentiation." Mechanisms of Development 126 (August 2009): S289—S290. http://dx.doi.org/10.1016/j.mod.2009.06.784.

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27

Okada, Norihisa, Yoko Ishigami, Takuji Suzuki, Akihiro Kaneko, Kensuke Yasui, Ryuuta Fukutomi, and Mamoru Isemura. "Importins and exportins in cellular differentiation." Journal of Cellular and Molecular Medicine 12, no. 5b (July 24, 2008): 1863–71. http://dx.doi.org/10.1111/j.1582-4934.2008.00437.x.

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28

Wada, Takeo, Sandrine Wallerich, and Attila Becskei. "Stochastic Gene Choice during Cellular Differentiation." Cell Reports 24, no. 13 (September 2018): 3503–12. http://dx.doi.org/10.1016/j.celrep.2018.08.074.

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29

Graham, Anthony. "Developmental homoplasy: convergence in cellular differentiation." Journal of Anatomy 216, no. 6 (March 30, 2010): 651–55. http://dx.doi.org/10.1111/j.1469-7580.2010.01232.x.

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30

IIJIMA, MISA. "CELLULAR DIFFERENTIATION AND PROLIFERATION IN MEDULLOBLASTOMA." KITAKANTO Medical Journal 46, no. 6 (1996): 471–82. http://dx.doi.org/10.2974/kmj1951.46.471.

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31

Narula, Jatin, Anna Kuchina, Fang Zhang, Masaya Fujita, Gürol M. Süel, and Oleg A. Igoshin. "Slowdown of growth controls cellular differentiation." Molecular Systems Biology 12, no. 5 (May 2016): 871. http://dx.doi.org/10.15252/msb.20156691.

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32

Bock, Susan C., Karlene Campo, and Marian R. Goldsmith. "Specific protein synthesis in cellular differentiation." Developmental Biology 117, no. 1 (September 1986): 215–25. http://dx.doi.org/10.1016/0012-1606(86)90364-7.

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33

Gaynor, R., K. Simon, and P. Koeffler. "Expression of c-jun during macrophage differentiation of HL-60 cells." Blood 77, no. 12 (June 15, 1991): 2618–23. http://dx.doi.org/10.1182/blood.v77.12.2618.2618.

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Abstract Cellular transcription factors are important in the regulation of cellular genes. Recent studies have indicated that a class of cellular genes known as early response genes are important in the control of cellular growth properties. Two of these genes, c-jun and c-fos, play an important role in the control of cellular differentiation. Because the acute myelogenous leukemia cell line, HL-60, is capable of differentiating to either macrophages or granulocytes, it provides a good model to understand differential gene expression. To determine if the modulation of c-jun was important in the differentiation of HL-60 cells to either macrophages or granulocytes, expression of c-jun mRNA was determined by Northern analysis at various times following treatment with a variety of differentiating agents, including 12- tetradeconyl-phorbol 13-acetate (TPA), retinoic acid (RA), dimethyl sulfoxide (DMSO), or 1,25 dihydroxyvitamin D3 [1,25 (OH)2 D3]. Both TPA and 1,25(OH)2D3, which induce HL-60 cells to differentiate to macrophages, resulted in marked increases in c-jun mRNA; while RA and DMSO, which induce HL-60 cells to differentiate to granulocytes, did not greatly alter c-jun mRNA expression. HL-60 cell lines resistant to macrophage differentiation after exposure to either 1,25(OH)2D3 or TPA did not result in increases in c-jun mRNA. These results suggest that elevation of c-jun mRNA in HL-60 cells correlated temporally with differentiation to macrophages. Thus, c-jun may be a critical cellular transcription factor involved in macrophage differentiation.

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34

Gaynor, R., K. Simon, and P. Koeffler. "Expression of c-jun during macrophage differentiation of HL-60 cells." Blood 77, no. 12 (June 15, 1991): 2618–23. http://dx.doi.org/10.1182/blood.v77.12.2618.bloodjournal77122618.

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Cellular transcription factors are important in the regulation of cellular genes. Recent studies have indicated that a class of cellular genes known as early response genes are important in the control of cellular growth properties. Two of these genes, c-jun and c-fos, play an important role in the control of cellular differentiation. Because the acute myelogenous leukemia cell line, HL-60, is capable of differentiating to either macrophages or granulocytes, it provides a good model to understand differential gene expression. To determine if the modulation of c-jun was important in the differentiation of HL-60 cells to either macrophages or granulocytes, expression of c-jun mRNA was determined by Northern analysis at various times following treatment with a variety of differentiating agents, including 12- tetradeconyl-phorbol 13-acetate (TPA), retinoic acid (RA), dimethyl sulfoxide (DMSO), or 1,25 dihydroxyvitamin D3 [1,25 (OH)2 D3]. Both TPA and 1,25(OH)2D3, which induce HL-60 cells to differentiate to macrophages, resulted in marked increases in c-jun mRNA; while RA and DMSO, which induce HL-60 cells to differentiate to granulocytes, did not greatly alter c-jun mRNA expression. HL-60 cell lines resistant to macrophage differentiation after exposure to either 1,25(OH)2D3 or TPA did not result in increases in c-jun mRNA. These results suggest that elevation of c-jun mRNA in HL-60 cells correlated temporally with differentiation to macrophages. Thus, c-jun may be a critical cellular transcription factor involved in macrophage differentiation.

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35

Pfaender, Stefanie, Karl Föhr, Anne-Kathrin Lutz, Stefan Putz, Kevin Achberger, Leonhard Linta, Stefan Liebau, Tobias M. Boeckers, and Andreas M. Grabrucker. "Cellular Zinc Homeostasis Contributes to Neuronal Differentiation in Human Induced Pluripotent Stem Cells." Neural Plasticity 2016 (2016): 1–15. http://dx.doi.org/10.1155/2016/3760702.

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Disturbances in neuronal differentiation and function are an underlying factor of many brain disorders. Zinc homeostasis and signaling are important mediators for a normal brain development and function, given that zinc deficiency was shown to result in cognitive and emotional deficits in animal models that might be associated with neurodevelopmental disorders. One underlying mechanism of the observed detrimental effects of zinc deficiency on the brain might be impaired proliferation and differentiation of stem cells participating in neurogenesis. Thus, to examine the molecular mechanisms regulating zinc metabolism and signaling in differentiating neurons, using a protocol for motor neuron differentiation, we characterized the expression of zinc homeostasis genes during neurogenesis using human induced pluripotent stem cells (hiPSCs) and evaluated the influence of altered zinc levels on the expression of zinc homeostasis genes, cell survival, cell fate, and neuronal function. Our results show that zinc transporters are highly regulated genes during neuronal differentiation and that low zinc levels are associated with decreased cell survival, altered neuronal differentiation, and, in particular, synaptic function. We conclude that zinc deficiency in a critical time window during brain development might influence brain function by modulating neuronal differentiation.

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36

Davidson, Gary, Rosanna Dono, and Rolf Zeller. "FGF signalling is required for differentiation-induced cytoskeletal reorganisation and formation of actin-based processes by podocytes." Journal of Cell Science 114, no. 18 (September 15, 2001): 3359–66. http://dx.doi.org/10.1242/jcs.114.18.3359.

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To examine the potential role of fibroblast growth factor (FGF) signalling during cell differentiation, we used conditionally immortalised podocyte cells isolated from kidneys of Fgf2 mutant and wild-type mice. Wild-type mouse podocyte cells upregulate FGF2 expression when differentiating in culture, as do maturing podocytes in vivo. Differentiating wild-type mouse podocyte cells undergo an epithelial to mesenchymal-like transition, reorganise their actin cytoskeleton and extend actin-based cellular processes; all of these activities are similar to the activity of podocytes in vivo. Molecular analysis of Fgf2 mutant mouse podocyte cells reveals a general disruption of FGF signalling as expression of Fgf7 and Fgf10 are also downregulated. These FGF mutant mouse podocyte cells in culture fail to activate mesenchymal markers and their post-mitotic differentiation is blocked. Furthermore, mutant mouse podocyte cells in culture fail to reorganise their actin cytoskeleton and form actin-based cellular processes. These studies show that FGF signalling is required by cultured podocytes to undergo the epithelial to mesenchymal-like changes necessary for terminal differentiation. Together with other studies, these results point to a general role for FGF signalling in regulating cell differentiation and formation of actin-based cellular processes during morphogenesis.

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37

Callens, Celine, Séverine Coulon, Jerome Naudin, Isabelle Radford-Weiss, Nicolas Boissel, Emmanuel Raffoux, Pamella Huey Mei Wang, et al. "Targeting iron homeostasis induces cellular differentiation and synergizes with differentiating agents in acute myeloid leukemia." Journal of Experimental Medicine 207, no. 4 (April 5, 2010): 731–50. http://dx.doi.org/10.1084/jem.20091488.

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Differentiating agents have been proposed to overcome the impaired cellular differentiation in acute myeloid leukemia (AML). However, only the combinations of all-trans retinoic acid or arsenic trioxide with chemotherapy have been successful, and only in treating acute promyelocytic leukemia (also called AML3). We show that iron homeostasis is an effective target in the treatment of AML. Iron chelating therapy induces the differentiation of leukemia blasts and normal bone marrow precursors into monocytes/macrophages in a manner involving modulation of reactive oxygen species expression and the activation of mitogen-activated protein kinases (MAPKs). 30% of the genes most strongly induced by iron deprivation are also targeted by vitamin D3 (VD), a well known differentiating agent. Iron chelating agents induce expression and phosphorylation of the VD receptor (VDR), and iron deprivation and VD act synergistically. VD magnifies activation of MAPK JNK and the induction of VDR target genes. When used to treat one AML patient refractory to chemotherapy, the combination of iron-chelating agents and VD resulted in reversal of pancytopenia and in blast differentiation. We propose that iron availability modulates myeloid cell commitment and that targeting this cellular differentiation pathway together with conventional differentiating agents provides new therapeutic modalities for AML.

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38

Yien, Yvette Y., Caiyong Chen, Jiahai Shi, Liangtao Li, Daniel E. Bauer, Nicholas Huston, Paul D. Kingsley, et al. "Fam210b Is Required for Optimal Cellular and Mitochondrial Iron Uptake during Erythroid Differentiation." Blood 126, no. 23 (December 3, 2015): 405. http://dx.doi.org/10.1182/blood.v126.23.405.405.

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Abstract Red cells synthesize large quantities of heme during terminal differentiation. Central to erythropoiesis is the transport and trafficking of iron within the cell. Despite the importance of iron transport during erythroid heme synthesis, the molecules involved in intracellular trafficking of iron are largely unknown. In a screen for genes that are up-regulated during erythroid terminal differentiation, we identified FAM210B, a predicted multi-pass transmembrane mitochondrial protein as an essential component of mitochondrial iron transport during erythroid differentiation. In zebrafish and mice, Fam210b mRNA is enriched in differentiating erythroid cells and liver (fetal and adult), which are tissues that require large amounts of iron for heme synthesis. Here, we report that FAM210B facilitates mitochondrial iron import during erythroid differentiation and is essential for hemoglobin synthesis. Zebrafish are anemic when fam210b is silenced using anti-sense morpholinos (Fig. A). CRISPR knockout of Fam210b caused a heme synthesis defect in differentiating Friend murine erythroleukemia (MEL) cells. PPIX levels in Fam210b deficient cells are normal, demonstrating that Fam210b does not participate in synthesis of the heme tetrapyrrole ring. Consistent with this result, supplementation of Fam210b deficient MEL cells with either aminolevulinic acid, the first committed substrate of the heme synthesis pathway or a chemical analog of protoporphyrin IX failed to chemically complement the heme synthesis defect. While Fam210b was not required for basal housekeeping heme synthesis, Fam210b deficientcells showed defective total cellular and mitochondrial iron uptake during erythroid differentiation (Fig. B). As a result, Fam210b deficient cells had defective hemoglobinization. Supplementation of Fam210b-/- MEL cells with non-transferrin iron chelates restored erythroid differentiation and hemoglobin synthesis; whereas, similar chemical complementation could not be achieved in the Tmem14c-/- cells, which have a primary defect in tetrapyrrole transport. (Fig. C). Our findings reveal that FAM210B is required for optimal mitochondrial iron import during erythroid differentiation for hemoglobin synthesis. It may therefore function as a genetic modifier for mitochondriopathies, anemias or porphyrias. Figure 1. Figure 1. Disclosures Bauer: Biogen: Research Funding; Editas Medicine: Consultancy. Orkin:Editas Inc.: Consultancy.

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39

Neubert, D. "Toxicity studies with cellular models of differentiation." Xenobiotica 15, no. 8-9 (January 1985): 649–60. http://dx.doi.org/10.3109/00498258509047423.

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40

Faenza, Irene. "Nuclear phospholipase C beta1 and cellular differentiation." Frontiers in Bioscience 13, no. 13 (2008): 2452. http://dx.doi.org/10.2741/2858.

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41

Snyder, Rhett A., Courtney K. Ellison, Geoffrey B. Severin, Gregory B. Whitfield, Christopher M. Waters, and Yves V. Brun. "Surface sensing stimulates cellular differentiation inCaulobacter crescentus." Proceedings of the National Academy of Sciences 117, no. 30 (July 13, 2020): 17984–91. http://dx.doi.org/10.1073/pnas.1920291117.

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Cellular differentiation is a fundamental strategy used by cells to generate specialized functions at specific stages of development. The bacteriumCaulobacter crescentusemploys a specialized dimorphic life cycle consisting of two differentiated cell types. How environmental cues, including mechanical inputs such as contact with a surface, regulate this cell cycle remain unclear. Here, we find that surface sensing by the physical perturbation of retracting extracellular pilus filaments accelerates cell-cycle progression and cellular differentiation. We show that physical obstruction of dynamic pilus activity by chemical perturbation or by a mutation in the outer-membrane pilus secretin CpaC stimulates early initiation of chromosome replication. In addition, we find that surface contact stimulates cell-cycle progression by demonstrating that surface-stimulated cells initiate early chromosome replication to the same extent as planktonic cells with obstructed pilus activity. Finally, we show that obstruction of pilus retraction stimulates the synthesis of the cell-cycle regulator cyclic diguanylate monophosphate (c-di-GMP) through changes in the activity and localization of two key regulatory histidine kinases that control cell fate and differentiation. Together, these results demonstrate that surface contact and sensing by alterations in pilus activity stimulateC. crescentusto bypass its developmentally programmed temporal delay in cell differentiation to more quickly adapt to a surface-associated lifestyle.

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42

Orza, Anamaria I., Carmen Mihu, Olga Soritau, Mircea Diudea, Adrian Florea, Horea Matei, Stefana Balici, Thilak Mudalige, Ganesh K. Kanarpardy, and Alexandru S. Biris. "Multistructural biomimetic substrates for controlled cellular differentiation." Nanotechnology 25, no. 6 (January 16, 2014): 065102. http://dx.doi.org/10.1088/0957-4484/25/6/065102.

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43

JAENISCH, R., K. HOCHEDLINGER, R. BLELLOCH, Y. YAMADA, K. BALDWIN, and K. EGGAN. "Nuclear Cloning, Epigenetic Reprogramming, and Cellular Differentiation." Cold Spring Harbor Symposia on Quantitative Biology 69 (January 1, 2004): 19–28. http://dx.doi.org/10.1101/sqb.2004.69.19.

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44

Molavi Kakhki, Arash, Abbas Razaghpanah, Rajesh Golani, David Choffnes, Phillipa Gill, and Alan Mislove. "Identifying traffic differentiation on cellular data networks." ACM SIGCOMM Computer Communication Review 44, no. 4 (February 25, 2015): 119–20. http://dx.doi.org/10.1145/2740070.2631445.

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45

Ryu, Stacy H., Gerard E. Kaiko, and Thaddeus S. Stappenbeck. "Cellular differentiation: Potential insight into butyrate paradox?" Molecular & Cellular Oncology 5, no. 3 (February 27, 2018): e1212685. http://dx.doi.org/10.1080/23723556.2016.1212685.

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46

Pyke, Kevin, and Enrique López-Juez. "Cellular Differentiation and Leaf Morphogenesis in Arabdopsis." Critical Reviews in Plant Sciences 18, no. 4 (July 1999): 527–46. http://dx.doi.org/10.1080/07352689991309388.

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47

Rippka, R., and M. Herdman. "Division patterns and cellular differentiation in cyanobacteria." Annales de l'Institut Pasteur / Microbiologie 136, no. 1 (January 1985): 33–39. http://dx.doi.org/10.1016/s0769-2609(85)80018-1.

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48

Silva, H. S., and M. L. Martins. "A cellular automata model for cell differentiation." Physica A: Statistical Mechanics and its Applications 322 (May 2003): 555–66. http://dx.doi.org/10.1016/s0378-4371(02)01807-1.

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49

Williams, Jeffrey G. "Regulation of cellular differentiation during dictyostelium morphogenesis." Current Opinion in Genetics & Development 1, no. 3 (October 1991): 358–62. http://dx.doi.org/10.1016/s0959-437x(05)80300-4.

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50

Smith, J. A. "Molecular mechanisms in cellular growth and differentiation." FEBS Letters 293, no. 1-2 (November 1, 1991): 227. http://dx.doi.org/10.1016/0014-5793(91)81198-h.

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