<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Prieto, Javier</style></author><author><style face="normal" font="default" size="100%">León, Marian</style></author><author><style face="normal" font="default" size="100%">Ponsoda, Xavier</style></author><author><style face="normal" font="default" size="100%">Garcia-Garcia, Francisco</style></author><author><style face="normal" font="default" size="100%">Bort, Roque</style></author><author><style face="normal" font="default" size="100%">Serna, Eva</style></author><author><style face="normal" font="default" size="100%">Barneo-Muñoz, Manuela</style></author><author><style face="normal" font="default" size="100%">Palau, Francesc</style></author><author><style face="normal" font="default" size="100%">Dopazo, Joaquin</style></author><author><style face="normal" font="default" size="100%">López-García, Carlos</style></author><author><style face="normal" font="default" size="100%">Torres, Josema</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Dysfunctional mitochondrial fission impairs cell reprogramming.</style></title><secondary-title><style face="normal" font="default" size="100%">Cell Cycle</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Cell Cycle</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Cycle Checkpoints</style></keyword><keyword><style  face="normal" font="default" size="100%">Cellular Reprogramming</style></keyword><keyword><style  face="normal" font="default" size="100%">DNA Damage</style></keyword><keyword><style  face="normal" font="default" size="100%">G2 Phase</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Knockdown Techniques</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice</style></keyword><keyword><style  face="normal" font="default" size="100%">Mitochondrial Dynamics</style></keyword><keyword><style  face="normal" font="default" size="100%">Mitosis</style></keyword><keyword><style  face="normal" font="default" size="100%">Nerve Tissue Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Pluripotent Stem Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Transcription Factors</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2016</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2016 Dec</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">15</style></volume><pages><style face="normal" font="default" size="100%">3240-3250</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;We have recently shown that mitochondrial fission is induced early in reprogramming in a Drp1-dependent manner; however, the identity of the factors controlling Drp1 recruitment to mitochondria was unexplored. To investigate this, we used a panel of RNAi targeting factors involved in the regulation of mitochondrial dynamics and we observed that MiD51, Gdap1 and, to a lesser extent, Mff were found to play key roles in this process. Cells derived from Gdap1-null mice were used to further explore the role of this factor in cell reprogramming. Microarray data revealed a prominent down-regulation of cell cycle pathways in Gdap1-null cells early in reprogramming and cell cycle profiling uncovered a G2/M growth arrest in Gdap1-null cells undergoing reprogramming. High-Content analysis showed that this growth arrest was DNA damage-independent. We propose that lack of efficient mitochondrial fission impairs cell reprogramming by interfering with cell cycle progression in a DNA damage-independent manner.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">23</style></issue><custom1><style face="normal" font="default" size="100%">https://www.ncbi.nlm.nih.gov/pubmed/27753531?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Manuel Iglesias, Juan</style></author><author><style face="normal" font="default" size="100%">Beloqui, Izaskun</style></author><author><style face="normal" font="default" size="100%">Garcia-Garcia, Francisco</style></author><author><style face="normal" font="default" size="100%">Leis, Olatz</style></author><author><style face="normal" font="default" size="100%">Vazquez-Martin, Alejandro</style></author><author><style face="normal" font="default" size="100%">Eguiara, Arrate</style></author><author><style face="normal" font="default" size="100%">Cufi, Silvia</style></author><author><style face="normal" font="default" size="100%">Pavon, Andres</style></author><author><style face="normal" font="default" size="100%">Menendez, Javier A</style></author><author><style face="normal" font="default" size="100%">Dopazo, Joaquin</style></author><author><style face="normal" font="default" size="100%">Martin, Angel G</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Mammosphere formation in breast carcinoma cell lines depends upon expression of E-cadherin.</style></title><secondary-title><style face="normal" font="default" size="100%">PLoS One</style></secondary-title><alt-title><style face="normal" font="default" size="100%">PLoS One</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Breast Neoplasms</style></keyword><keyword><style  face="normal" font="default" size="100%">Cadherins</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Line, Tumor</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Proliferation</style></keyword><keyword><style  face="normal" font="default" size="100%">Cluster Analysis</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">gene expression</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Expression Profiling</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Expression Regulation, Neoplastic</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Knockdown Techniques</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">MCF-7 Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Neoplastic Stem Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Spheroids, Cellular</style></keyword><keyword><style  face="normal" font="default" size="100%">Tumor Cells, Cultured</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2013</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2013</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">8</style></volume><pages><style face="normal" font="default" size="100%">e77281</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Tumors are heterogeneous at the cellular level where the ability to maintain tumor growth resides in discrete cell populations. Floating sphere-forming assays are broadly used to test stem cell activity in tissues, tumors and cell lines. Spheroids are originated from a small population of cells with stem cell features able to grow in suspension culture and behaving as tumorigenic in mice. We tested the ability of eleven common breast cancer cell lines representing the major breast cancer subtypes to grow as mammospheres, measuring the ability to maintain cell viability upon serial non-adherent passage. Only MCF7, T47D, BT474, MDA-MB-436 and JIMT1 were successfully propagated as long-term mammosphere cultures, measured as the increase in the number of viable cells upon serial non-adherent passages. Other cell lines tested (SKBR3, MDA-MB-231, MDA-MB-468 and MDA-MB-435) formed cell clumps that can be disaggregated mechanically, but cell viability drops dramatically on their second passage. HCC1937 and HCC1569 cells formed typical mammospheres, although they could not be propagated as long-term mammosphere cultures. All the sphere forming lines but MDA-MB-436 express E-cadherin on their surface. Knock down of E-cadherin expression in MCF-7 cells abrogated its ability to grow as mammospheres, while re-expression of E-cadherin in SKBR3 cells allow them to form mammospheres. Therefore, the mammosphere assay is suitable to reveal stem like features in breast cancer cell lines that express E-cadherin.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">10</style></issue><custom1><style face="normal" font="default" size="100%">https://www.ncbi.nlm.nih.gov/pubmed/24124614?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Carrero, Rubén</style></author><author><style face="normal" font="default" size="100%">Cerrada, Inmaculada</style></author><author><style face="normal" font="default" size="100%">Lledó, Elisa</style></author><author><style face="normal" font="default" size="100%">Dopazo, Joaquin</style></author><author><style face="normal" font="default" size="100%">Garcia-Garcia, Francisco</style></author><author><style face="normal" font="default" size="100%">Rubio, Mari-Paz</style></author><author><style face="normal" font="default" size="100%">Trigueros, César</style></author><author><style face="normal" font="default" size="100%">Dorronsoro, Akaitz</style></author><author><style face="normal" font="default" size="100%">Ruiz-Sauri, Amparo</style></author><author><style face="normal" font="default" size="100%">Montero, José Anastasio</style></author><author><style face="normal" font="default" size="100%">Sepúlveda, Pilar</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">IL1β induces mesenchymal stem cells migration and leucocyte chemotaxis through NF-κB.</style></title><secondary-title><style face="normal" font="default" size="100%">Stem Cell Rev Rep</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Stem Cell Rev Rep</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Cell Adhesion</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Movement</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Proliferation</style></keyword><keyword><style  face="normal" font="default" size="100%">Chemokines</style></keyword><keyword><style  face="normal" font="default" size="100%">Chemotaxis, Leukocyte</style></keyword><keyword><style  face="normal" font="default" size="100%">Collagen</style></keyword><keyword><style  face="normal" font="default" size="100%">Fibronectins</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Expression Profiling</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Knockdown Techniques</style></keyword><keyword><style  face="normal" font="default" size="100%">HEK293 Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">I-kappa B Kinase</style></keyword><keyword><style  face="normal" font="default" size="100%">Inflammation Mediators</style></keyword><keyword><style  face="normal" font="default" size="100%">Intercellular Signaling Peptides and Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Interleukin-1beta</style></keyword><keyword><style  face="normal" font="default" size="100%">Laminin</style></keyword><keyword><style  face="normal" font="default" size="100%">Leukocytes</style></keyword><keyword><style  face="normal" font="default" size="100%">Mesenchymal Stem Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">NF-kappa B</style></keyword><keyword><style  face="normal" font="default" size="100%">Oligonucleotide Array Sequence Analysis</style></keyword><keyword><style  face="normal" font="default" size="100%">RNA Interference</style></keyword><keyword><style  face="normal" font="default" size="100%">Signal Transduction</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2012</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2012 Sep</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">8</style></volume><pages><style face="normal" font="default" size="100%">905-16</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Mesenchymal stem cells are often transplanted into inflammatory environments where they are able to survive and modulate host immune responses through a poorly understood mechanism. In this paper we analyzed the responses of MSC to IL-1β: a representative inflammatory mediator. Microarray analysis of MSC treated with IL-1β revealed that this cytokine activateds a set of genes related to biological processes such as cell survival, cell migration, cell adhesion, chemokine production, induction of angiogenesis and modulation of the immune response. Further more detailed analysis by real-time PCR and functional assays revealed that IL-1β mainly increaseds the production of chemokines such as CCL5, CCL20, CXCL1, CXCL3, CXCL5, CXCL6, CXCL10, CXCL11 and CX(3)CL1, interleukins IL-6, IL-8, IL23A, IL32, Toll-like receptors TLR2, TLR4, CLDN1, metalloproteins MMP1 and MMP3, growth factors CSF2 and TNF-α, together with adhesion molecules ICAM1 and ICAM4. Functional analysis of MSC proliferation, migration and adhesion to extracellular matrix components revealed that IL-1β did not affect proliferation but also served to induce the secretion of trophic factors and adhesion to ECM components such as collagen and laminin. IL-1β treatment enhanced the ability of MSC to recruit monocytes and granulocytes in vitro. Blockade of NF-κβ transcription factor activation with IκB kinase beta (IKKβ) shRNA impaired MSC migration, adhesion and leucocyte recruitment, induced by IL-1β demonstrating that NF-κB pathway is an important downstream regulator of these responses. These findings are relevant to understanding the biological responses of MSC to inflammatory environments.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">3</style></issue><custom1><style face="normal" font="default" size="100%">https://www.ncbi.nlm.nih.gov/pubmed/22467443?dopt=Abstract</style></custom1></record></records></xml>