bluuebunny/crossref_metadata_2025_split huggingface dataset:
Specific replication factors are targeted by different genotoxic agents to inhibit replication
Authors: Sharma Aparna , Kar Ananya , Kaur Manpreet , Ranade Sourabh M. , Sankaran Aparna , Misra Shashank , Rawat Kanchan , Saxena Sandeep 
Published: October 2010

AbstractWhen mammalian cells experience DNA damaging stress, they block DNA replication to avoid erroneous replication of the damaged template. The cells that are unable to respond to DNA damage continue faulty DNA replication that results in incorporation of genomic lesions. To understand the regulation of replication machinery during stress, systemic studies have been carried out but they have been restricted to the evaluation of the mRNA levels and therefore have not been able to identify post‐transcriptional changes, vital for immediate blocking of the progressing DNA replication. We have recently discovered that an essential replication factor is downregulated by radiation stress. In this study, we have carried out a systematic evaluation of protein levels of entire replication apparatus after different types of DNA damage. We report that, independent of the status of p53 and retinoblastoma protein, mammalian cells choose targets that are essential for prereplication, preinitiation, and elongation phases of replication. We imposed different kinds of stress to discern whether similar or unique responses are invoked, and we propose a model for inhibition of replication machinery in which mammalian cells target specific essential replication factors based on the experienced stress. © 2010 IUBMB IUBMB Life, 62(10): 764–775, 2010
Improving the Wang–Landau algorithm for polymers and proteins
Authors: Swetnam Adam D. , Allen Michael P. 
Published: October 2010

AbstractThe 1/t Wang–Landau algorithm is tested on simple models of polymers and proteins. It is found that this method resolves the problem of the saturation of the error present in the original algorithm for lattice polymers. However, for lattice proteins, which have a rough energy landscape with an unknown energy minimum, it is found that the density of states does not converge in all runs. A new variant of the Wang–Landau algorithm that appears to solve this problem is described and tested. In the new variant, the optimum modification factor is calculated in the same straightforward way throughout the simulation. There is only one free parameter for which a value of unity appears to give near optimal convergence for all run lengths for lattice homopolymers when pull moves are used. For lattice proteins, a much smaller value of the parameter is needed to ensure rapid convergence of the density of states for energies discovered late in the simulation, which unfortunately results in poor convergence early on in the run. © 2010 Wiley Periodicals, Inc. J Comput Chem, 2011.
Cell surface N‐glycans‐mediated isolation of mouse neural stem cells
Authors: Hamanoue Makoto , Okano Hideyuki 
Published: October 2010

AbstractThe isolation of neural stem cells (NSCs) has been hampered by the lack of valid cell‐surface antigens on NSCs, and novel valuable markers have been proposed. Glycan (oligosaccharide chain) is a potential candidate as a marker to isolate NSCs, because the species and the combination order of saccharides in glycan generate remarkable structural diversity and specificity. At present, the expression of hundreds of glycoconjugates with glycans have been found in the NSCs; however, just a few glycan‐epitopes have been identified as valuable cell‐surface markers. This review focused on the isolation of NSC using glycoprotein, especially complex type N‐glycans. The cell‐surface N‐glycan‐mediated isolation of NSCs is therefore expected to provide a comprehensive understanding of the biologic characteristics of NSCs in the brain, and thereby help to develop novel strategies in the field of regenerative medicine. J. Cell. Physiol. 226: 1433–1438, 2011. © 2010 Wiley‐Liss, Inc.
PINCH: More than just an adaptor protein in cellular response
Authors: Kovalevich Jane , Tracy Brittany , Langford Dianne 
Published: October 2010

AbstractParticularly interesting new cysteine‐histidine‐rich protein (PINCH) is a LIM‐domain‐only adaptor protein involved in protein recruitment, subsequent assembly of multi‐protein complexes, and subcellular localization of these complexes. PINCH is developmentally regulated and its expression is critical for proper cytoskeletal organization and extracellular matrix adhesion. Although PINCH has no catalytic abilities, the PIP (PINCH–ILK–parvin) complex serves as a link between integrins and components of growth factor receptor kinase and GTPase signaling pathways. Accordingly, PINCH‐mediated signaling induces cell migration, spreading, and survival. Further research on the signaling cascades affected by PINCH is key to appreciating its biological significance in cell fate and systems maintenance, as the developmental functions of PINCH may extend to disease states and the cellular response to damage. PINCH is implicated in a diverse array of diseases including renal failure, cardiomyopathy, nervous system degeneration and demyelination, and tumorigenesis. This review presents evidence for PINCH's structural and functional importance in normal cellular processes and in pathogenesis. The current data for PINCH expression in nervous system disease is substantial, but due to the complex and ubiquitous nature of this protein, our understanding of its function in pathology remains unclear. In this review, an overview of studies identifying PINCH binding partners, their molecular interactions, and the potentially overlapping role(s) of PINCH in cancer and in nervous system diseases will be discussed. Many questions remain regarding PINCH's role in cells. What induces cell‐specific PINCH expression? How does PINCH expression contribute to cell fate in the central nervous system? More broadly, is PINCH expression in disease a good thing? Clarifying the ambiguous functions of PINCH expression in the central nervous system and other systems is important to understand more clearly signaling events both in health and disease. J. Cell. Physiol. 226: 940–947, 2011. © 2010 Wiley‐Liss, Inc.
The relationship between the Wnt/β‐catenin and TGF‐β/BMP signals in the intervertebral disc cell
Authors: Hiyama Akihiko , Sakai Daisuke , Tanaka Masahiro , Arai Fumiyuki , Nakajima Daisuke , Abe Koichiro , Mochida Joji 
Published: October 2010

AbstractDegeneration of the lumbar intervertebral disc (IVD) is a cause of low back pain. In osteoarthritis patients, an increase in β‐catenin accumulation has been reported. However, the molecular mechanisms involved in IVD remain unclear. In the present study, we examined the relationship of Wnt/β‐catenin and transforming growth factor‐β (TGF‐β)/bone morphogenetic protein (BMP) signals in the IVDs. We found that treatment of nucleus pulposus (NP) cells with the Wnt/β‐catenin activator lithium chloride (LiCl) results in the increased expression of β‐catenin mRNA and protein, and cell proliferation is decreased due to the activation of the Wnt/β‐catenin signals through the suppression of c‐myc and cyclin‐D1. In addition, T‐cell‐specific transcription factor (TCF) promoter activity was found to increase the following stimulation with LiCl alone, and was further increased when BMP2 was added, in comparison to the control group. We further observed the effects of treatment with PD98059, a specific inhibitor of the mitogen‐activated protein kinase pathway, on TCF promoter activity in NP cells. These effects were largely attenuated by PD98059. Moreover, when transfected IVDs were co‐transfected with R‐Smad expression plasmids, there was a significant decrease in TCF reporter activity. We thereafter evaluated the effects of increased Wnt/β‐catenin activity on the transcriptional activity of the Smad binding element (SBE). As a result, LiCl suppressed the activity of SBE reporter activity. The present study demonstrates for the first time that there are opposing effects between the Wnt/β‐catenin and TGF‐β/BMP signals in IVDs, which is consistent with the Wnt/β‐catenin signals contributing to the pathogenesis of IVD degeneration. J. Cell. Physiol. 226: 1139–1148, 2011. © 2010 Wiley‐Liss, Inc.
Nestin(+) stem cells independently contribute to neural remodelling of the ischemic heart
Authors: Béguin Pauline C. , El‐Helou Viviane , Gillis Marc‐Antoine , Duquette Natacha , Gosselin Hugues , Brugada Ramon , Villeneuve Louis , Lauzier Dominique , Tanguay Jean‐Francois , Ribuot Christophe , Calderone Angelino 
Published: October 2010

AbstractRecent studies have revealed the existence of multipotent nestin‐immunoreactive cells in the adult mammalian heart. These cells were recruited to infarct site following ischemic injury and differentiated to a vascular lineage leading to de novo blood vessel formation. Here, we show that a sub‐population of cardiac resident nestin(+) cells can further differentiate to a neuronal‐like fate in vivo following myocardial infarction. In the ischemically damaged rat heart, neurofilament‐M(+) fibres were detected innervating the peri‐infarct/infarct region and the preponderance of these fibres were physically associated with processes emanating from nestin(+) cells. One week after isogenic heterotopic cardiac transplantation, the beating transplanted rat heart was devoid of neurofilament‐M(+) fibre staining. The superimposition of an ischemic insult to the transplanted heart led to the de novo synthesis of neurofilament‐M(+) fibres by cardiac resident nestin(+) cells. Nerve growth factor infusion and the exposure of normal rats to intermittent hypoxia significantly increased the density of neurofilament‐M(+) fibres in the heart. However, these newly formed neurofilament‐M(+) fibres were not physically associated with nestin(+) processes. These data highlight a novel paradigm of reparative fibrosis as a subpopulation of cardiac resident nestin(+) cells directly contributed to neural remodelling of the peri‐infarct/infarct region of the ischemically damaged rat heart via the de novo synthesis of neurofilament‐M fibres. J. Cell. Physiol. 226: 1157–1165, 2011. © 2010 Wiley‐Liss, Inc.
Lack of association between stretch‐activated and volume‐activated Cl− currents in hepatocellular carcinoma cells
Authors: Mao Jianwen , Xu Bin , Li Hongzhi , Chen Lixin , Jin Xiaobao , Zhu Jiayong , Wang Weizhang , Zhu Linyan , Zuo Wanhong , Chen Weiqiang , Wang Liwei 
Published: October 2010

AbstractStretch‐activated chloride currents (ICl,SA) have been considered to be a component of volume‐activated chloride currents (ICl,vol) for some time. This is due to a similarity in biophysical and pharmacological properties that involve a membrane curvature‐induced mechanism and rearrangement of the cytoskeleton induced by cell swelling or membrane stretch. In the present study, we demonstrated that current density, along with the time taken from the activation of currents to the peak, were significantly different between the two currents, in highly metastatic human hepatocellular carcinoma cells. In addition, the activation of ICl,vol or ICl,SA, induced maximally by hypotonic solutions or membrane stretch, respectively, did not affect the following activation of the other one. Moreover, neither inhibition of ICl,vol by sh‐ClC‐3 transfection, nor functional blocking of ICl,vol by intracellular dialysis of anti‐ClC‐3 antibody had an effect on the activation and properties of ICl,SA. Collectively, our results suggest that ICl,SA is different from ICl,vol in activation mechanism and/or in molecular entity responsible for formation of the currents. ClC‐3 is involved in the activation of ICl,vol, but not of ICl,SA. J. Cell. Physiol. 226: 1176–1185, 2011. © 2010 Wiley‐Liss, Inc.
Mechanistic insights into reprogramming to induced pluripotency
Authors: Ho Ritchie , Chronis Constantinos , Plath Kathrin 
Published: October 2010

AbstractInduced pluripotent stem (iPS) cells can be generated from various embryonic and adult cell types upon expression of a set of few transcription factors, most commonly consisting of Oct4, Sox2, cMyc, and Klf4, following a strategy originally published by Takahashi and Yamanaka (Takahashi and Yamanaka, 2006, Cell 126: 663–676). Since iPS cells are molecularly and functionally similar to embryonic stem (ES) cells, they provide a source of patient‐specific pluripotent cells for regenerative medicine and disease modeling, and therefore have generated enormous scientific and public interest. The generation of iPS cells also presents a powerful tool for dissecting mechanisms that stabilize the differentiated state and are required for the establishment of pluripotency. In this review, we discuss our current view of the molecular mechanisms underlying transcription factor‐mediated reprogramming to induced pluripotency. J. Cell. Physiol. 226: 868–878, 2011. © 2010 Wiley‐Liss, Inc.
Vasodilator‐stimulated phosphoprotein deficiency potentiates PAR‐1‐induced increase in endothelial permeability in mouse lungs
Authors: Profirovic Jasmina , Han Jingyan , Andreeva Alexandra V. , Neamu Radu F. , Pavlovic Sasha , Vogel Stephen M. , Walter Ulrich , Voyno‐Yasenetskaya Tatyana A. 
Published: October 2010

AbstractVasodilator‐stimulated phosphoprotein (VASP) is implicated in the protection of the endothelial barrier in vitro and in vivo. The function of VASP in thrombin signaling in the endothelial cells (ECs) is not known. For the first time we studied the effects of VASP deficiency on EC permeability and pulmonary vascular permeability in response to thrombin receptor stimulation. We provided the evidence that VASP deficiency potentiates the increase in endothelial permeability induced by activation of thrombin receptor in cultured human umbilical vein endothelial cells (HUVECs) and isolated mouse lungs. Using transendothelial resistance measurement, we showed that siRNA‐mediated VASP downregulation in HUVECs leads to a potentiation of thrombin‐ and protease‐activated receptor 1 (PAR‐1) agonist‐induced increase in endothelial permeability. Compared to control cells, VASP‐deficient HUVECs had delayed endothelial junctional reassembly and abrogated VE‐cadherin cytoskeletal anchoring in the recovery phase after thrombin stimulation, as demonstrated by immunofluorescence studies and cell fractionation analysis, respectively. Measurement of the capillary filtration coefficient in isolated mouse lungs demonstrated that VASP−/− mice have increased microvascular permeability in response to infusion with PAR‐1 agonist compared to wild type mice. Lack of VASP led to decreased Rac1 activation both in VASP‐deficient HUVECs after thrombin stimulation and VASP−/− mouse lungs after PAR‐1 agonist infusion, indicating that VASP effects on thrombin signaling may be correlated with changes in Rac1 activity. This study demonstrates that VASP may play critical and complex role in the regulation of thrombin‐dependent disruption of the endothelial barrier function. J. Cell. Physiol. 226: 1255–1264, 2011. © 2010 Wiley‐Liss, Inc.
On the role of subtype selective adenosine receptor agonists during proliferation and osteogenic differentiation of human primary bone marrow stromal cells
Authors: Costa M. Adelina , Barbosa A. , Neto E. , Sá‐e‐Sousa A. , Freitas R. , Neves J.M. , Magalhães‐Cardoso T. , Ferreirinha F. , Correia‐de‐Sá P. 
Published: October 2010

AbstractPurines are important modulators of bone cell biology. ATP is metabolized into adenosine by human primary osteoblast cells (HPOC); due to very low activity of adenosine deaminase, the nucleoside is the end product of the ecto‐nucleotidase cascade. We, therefore, investigated the expression and function of adenosine receptor subtypes (A1, A2A, A2B, and A3) during proliferation and osteogenic differentiation of HPOC. Adenosine A1(CPA), A2A(CGS21680C), A2B(NECA), and A3(2‐Cl‐IB‐MECA) receptor agonists concentration‐dependently increased HPOC proliferation. Agonist‐induced HPOC proliferation was prevented by their selective antagonists, DPCPX, SCH442416, PSB603, and MRS1191. CPA and NECA facilitated osteogenic differentiation measured by increases in alkaline phosphatase (ALP) activity. This contrasts with the effect of CGS21680C which delayed HPOC differentiation; 2‐Cl‐IB‐MECA was devoid of effect. Blockade of the A2Breceptor with PSB603 prevented osteogenic differentiation by NECA. In the presence of the A1antagonist, DPCPX, CPA reduced ALP activity at 21 and 28 days in culture. At the same time points, blockade of A2Areceptors with SCH442416 transformed the inhibitory effect of CGS21680C into facilitation. Inhibition of adenosine uptake with dipyridamole caused a net increase in osteogenic differentiation. The presence of all subtypes of adenosine receptors on HPOC was confirmed by immunocytochemistry. Data show that adenosine is an important regulator of osteogenic cell differentiation through the activation of subtype‐specific receptors. The most abundant A2Breceptor seems to have a consistent role in cell differentiation, which may be balanced through the relative strengths of A1or A2Areceptors determining whether osteoblasts are driven into proliferation or differentiation. J. Cell. Physiol. 226: 1353–1366, 2011. © 2010 Wiley‐Liss, Inc.
Constitutive overexpression of Id‐1 in mammary glands of transgenic mice results in precocious and increased formation of terminal end buds, enhanced alveologenesis, delayed involution
Authors: Shin Dong‐Hui , Jang Si‐Hyong , Kang Byeong‐Cheol , Kim Hyun‐Jun , Oh Seung Hyun , Kong Gu 
Published: October 2010

AbstractInhibitor of differentiation‐1 (Id‐1) has been shown to play an essential role in cell proliferation, invasion, migration, and anti‐apoptosis. However, the effect of Id‐1 in mammary gland development remains unknown. Here, we generated MMTV‐Id‐1 transgenic mice to study the role of Id‐1 in mammary gland development. In virgin mice, Id‐1 overexpression led to precocious development and delayed regression of terminal end buds (TEBs) compared with wild‐type mice. The number of BrdU‐positive cells and the expression of Wnt signaling molecules, β‐catenin and cyclin D1, which regulate ductal extension and TEB formation in virgin, were statistically higher in Id‐1 transgenic mice than in wild‐type mice. Id‐1 also had an effect on the formation and proliferation of lobuloalveolar structures during early and mid‐pregnancy. Id‐1 transgenic mice had more lobulated and prominent alveolar budding than wild‐type mice and had significantly greater counts of lobuloalveolar structures in early pregnancy. The expression of BrdU, β‐catenin, and cyclin D1 was also predominantly increased in Id‐1 transgenic mice. Moreover, Id‐1 transgenic mice showed delayed involution. Id‐1 regulated the expression levels of anti‐apoptotic Bcl‐2 and pro‐apoptotic Bax, and resulted in delay of apoptotic peak during postlactational involution. We also found that Id‐1 was able to modulate expression of the regulators of Wnt/β‐catenin signaling such as phospho‐Akt, BMP2, FGF3, and RAR‐β in tubuloalveolar development of mammary glands. Taken together, our results suggest that Id‐1 plays a pivotal role in mammary gland development through Wnt signaling‐mediated acceleration of precocity and alveologenesis and Bcl‐2 family members‐mediated delay of involution. J. Cell. Physiol. 226: 1340–1352, 2011. © 2010 Wiley‐Liss, Inc.
Embryonal carcinoma cell induction of miRNA and mRNA changes in co‐cultured prostate stromal fibromuscular cells
Authors: Vêncio Eneida F. , Pascal Laura E. , Page Laura S. , Denyer Gareth , Wang Amy J. , Ruohola‐Baker Hannele , Zhang Shile , Wang Kai , Galas David J. , Liu Alvin Y. 
Published: October 2010

AbstractThe prostate stromal mesenchyme controls organ‐specific development. In cancer, the stromal compartment shows altered gene expression compared to non‐cancer. The lineage relationship between cancer‐associated stromal cells and normal tissue stromal cells is not known. Nor is the cause underlying the expression difference. Previously, the embryonal carcinoma (EC) cell line, NCCIT, was used by us to study the stromal induction property. In the current study, stromal cells from non‐cancer (NP) and cancer (CP) were isolated from tissue specimens and co‐cultured with NCCIT cells in a trans‐well format to preclude heterotypic cell contact. After 3 days, the stromal cells were analyzed by gene arrays for microRNA (miRNA) and mRNA expression. In co‐culture, NCCIT cells were found to alter the miRNA and mRNA expression of NP stromal cells to one like that of CP stromal cells. In contrast, NCCIT had no significant effect on the gene expression of CP stromal cells. We conclude that the gene expression changes in stromal cells can be induced by diffusible factors synthesized by EC cells, and suggest that cancer‐associated stromal cells represent a more primitive or less differentiated stromal cell type. J. Cell. Physiol. 226: 1479–1488, 2011. © 2010 Wiley‐Liss, Inc.
Protein acetylation within the cellular response to radiation
Authors: Averbeck Nicole B. , Durante Marco 
Published: October 2010

AbstractPost‐translational protein modification represents a fundamental tool within the control of protein functions. While phosphorylation is the longest known of these modifications, several more were identified. Among these, acetylation was originally discovered as an important modification of histones within the process of transcription. Later it was revealed that histone acetylation also plays a crucial role in DNA repair, and that histones are not the only target for transient acetylation within these processes. Although there is no doubt that protein acetylation is essential, its function and even more its regulation is still not fully elucidated. Here we will discuss how protein acetylation occurs within the cellular response to radiation, a well characterized DNA‐damaging environmental stressor and further want to draw the attention to open questions within the field of protein acetylation. J. Cell. Physiol. 226: 962–967, 2011. © 2010 Wiley‐Liss, Inc.
A comprehensive characterization study of human bone marrow mscs with an emphasis on molecular and ultrastructural properties
Authors: Karaöz Erdal , Okçu Alparslan , Gacar Gülçin , Sağlam Özlem , Yürüker Sinan , Kenar Halime 
Published: October 2010

AbstractHuman bone marrow‐derived mesenchymal stem cells (hBM‐MSCs) continue to draw attention of researchers in the fields of basic science and medicine due to their indispensible regenerative, reparative, angiogenic, anti‐apoptotic, and immunosuppressive properties, all of which collectively point out their enormous therapeutic potential. There is still, however, a need for further investigation of their characteristics to broaden their field of use and learn much more about how to control their fate and improve their therapeutic effectiveness. hBM‐MSCs were extensively characterized in terms of their growth characteristics, genetic stability, and differentiation capability to the mesodermal and ectodermal cell lineages; a special emphasis was given to their phenotypic and ultrastructural properties. Expression of embryonic stem cell markers Oct4, Rex‐1, FoxD‐3, Sox2, and Nanog was shown with real‐time PCR. Transmission electron microscopy revealed the ultrastructural characteristics of hBM‐MSCs; they had pale, irregularly shaped and large euchromatic nuclei, and two distinct areas in their cytoplasm: an intensely stained inner zone rich in mitochondria and rough endoplasmic reticulum (rER) with dilated cisternae and a relatively peripheral zone poor in organelles. hBM‐MSCs expressed adipogenic (adipophilin and PPARγ), myogenic (desmin, myogenin, α‐SMA), neurogenic (γ‐enolase, MAP2a,b, c‐fos, nestin, NF‐H, NF‐L, GFAP, β3‐tubulin), osteogenic (osteonectin, osteocalcin, osteopontin, Runx‐2, type I collagen), and chondrogenic (type II collagen, SOX9) markers either at RNA or protein level even under basal conditions, without any stimulation towards differentiation. The differentiation potential of hBM‐MSCs to adipogenic, osteogenic, and neurogenic lineages was shown by using the relevant differentiation factors. J. Cell. Physiol. 226: 1367–1382, 2011. © 2010 Wiley‐Liss, Inc.