G1-phase progression in pluripotent stem cells

Cellular and Molecular Life Sciences - During early embryonic development both the rapid increase in cell number and the expression of genes that control developmental decisions are tightly...     

Okinonellins A and B,two novel furanosesterterpenes,which inhibit cell division of fertilized starfish eggs,from the marine spongeSpongionella sp

Cellular and Molecular Life Sciences - Two novel furanosesterterpenes, okinonellins A (1) and B (2), have been isolated from the spongeSpongionella sp. Both compounds inhibit cell division of...     

Physiological and pathological consequences of cellular senescence

Cellular senescence, a permanent state of cell cycle arrest accompanied by a complex phenotype, is an essential mechanism that limits tumorigenesis and tissue damage. In physiological conditions, senescent cells can be removed by the immune system, facilitating tumor suppression and wound healing. However, as we age, senescent cells accumulate in tissues, either because an aging immune system fails to remove them, the rate of senescent cell formation is elevated, or both. If senescent cells persist in tissues, they have the potential to paradoxically promote pathological conditions. Cellular senescence is associated with an enhanced pro-survival phenotype, which most likely promotes persistence of senescent cells in vivo. This phenotype may have evolved to favor facilitation of a short-term wound healing, followed by the elimination of senescent cells by the immune system. In this review, we provide a perspective on the triggers, mechanisms and physiological as well as pathological consequences of senescent cells.     

HDAC2 and TXNL1 distinguish aneuploid from diploid colorectal cancers

DNA aneuploidy has been identified as a prognostic factor for epithelial malignancies. Further understanding of the translation of DNA aneuploidy into protein expression will help to define novel biomarkers to improve therapies and prognosis. DNA ploidy was assessed by image cytometry. Comparison of gel-electrophoresis-based protein expression patterns of three diploid and four aneuploid colorectal cancer cell lines detected 64 ploidy-associated proteins. Proteins were identified by mass spectrometry and subjected to Ingenuity Pathway Analysis resulting in two overlapping high-ranked networks maintaining Cellular Assembly and Organization, Cell Cycle, and Cellular Growth and Proliferation. CAPZA1, TXNL1, and HDAC2 were significantly validated by Western blotting in cell lines and the latter two showed expression differences also in clinical samples using a tissue microarray of normal mucosa (n?=?19), diploid (n?=?31), and aneuploid (n?=?47) carcinomas. The results suggest that distinct protein expression patterns, affecting TXNL1 and HDAC2, distinguish aneuploid with poor prognosis from diploid colorectal cancers.     

Mechanisms of endothelial cell migration

Cell migration plays a central role in a variety of physiological and pathological processes during our whole life. Cellular movement is a complex, tightly regulated multistep process. Although the principle mechanisms of migration follow a defined general motility cycle, the cell type and the context of moving influences the detailed mode of migration. Endothelial cells migrate during vasculogenesis and angiogenesis but also in a damaged vessel to restore vessel integrity. Depending on the situation they migrate individually, in chains or sheets and complex signaling, intercellular signals as well as environmental cues modulate the process. Here, the different modes of cell migration, the peculiarities of endothelial cell migration and specific guidance molecules controlling this process will be reviewed.     

Effects of retinoic acid on ascites cells of the TA3 mouse mammary carcinoma

Summary Retinoic acid caused a decrease in adhesiveness but no growth change in the allotransplantable TA3-Ha cell and no change in adhesiveness or growth in the strain specific TA3-St cell. The retinoic acid binding protein was detected in the TA3-Ha, but not the TA3-St, cell.This study was supported in pat by Public Health Service Grants CA-08418 and CA-18600 from the National Cancer Institute, National Institutes of Health. This is publication 955 of the Robert W. Lovett Group for the Study of Diseases Causing Deformities. We gratefully acknowledge the contributions of Drs Luigi M. De Luca and Anton M. Jetten of the Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, National Institutes of Health, Bethesda, MD, without whose help this study would not have been possible.     

Cellular copper distribution: a mechanistic systems biology approach

Copper is an essential but potentially harmful trace element required in many enzymatic processes involving redox chemistry. Cellular copper homeostasis in mammals is predominantly maintained by regulating copper transport through the copper import CTR proteins and the copper exporters ATP7A and ATP7B. Once copper is imported into the cell, several pathways involving a number of copper proteins are responsible for trafficking it specifically where it is required for cellular life, thus avoiding the release of harmful free copper ions. In this study we review recent progress made in understanding the molecular mechanisms of copper transport in cells by analyzing structural features of copper proteins, their mode of interaction, and their thermodynamic and kinetic parameters, thus contributing to systems biology of copper within the cell.     

Cellular communications in bone homeostasis and repair

Cellular communication between the bone component cells osteoblasts, osteocytes and (pre-)osteoclasts is essential for bone remodeling which maintains bone integrity. As in the remodeling of other organs, cell death is a trigger for remodeling of bone. During the systematic process of bone remodeling, direct or indirect cell–cell communication is indispensable. Thus, osteoblasts induce migration and differentiation of preosteoclasts, which is followed by bone resorption (by mature multinuclear osteoclasts). After completion of bone resorption, apoptosis of mature osteoclasts and differentiation of osteoblasts are initiated. At this time, the osteoblasts do not support osteoclast differentiation but do support bone formation. Finally, osteoblasts differentiate to osteocytes in bone or to bone lining cells on bone surfaces. In this way, old bone areas are regenerated as new bone. In this review the role of cell–cell communication in bone remodeling is discussed.     

Concluding remarks

Cellular and Molecular Life Sciences -     

Sterol metabolism in insects and biosynthesis of ecdysone in the silkworm

Cellular and Molecular Life Sciences -     

Reactivity of enterovirus specific immunoglobulin M and G antibodies from sera of echovirus 11 infected newborns

Cellular and Molecular Life Sciences -     

Teratologische Prüfung einiger Thalidomid-Metabolite

Cellular and Molecular Life Sciences -     

Conformational studies oncyclohexanones

Cellular and Molecular Life Sciences -     

Isolation ofAeromonas spp. from human feces

Cellular and Molecular Life Sciences -     

Focusing on phosphomonohydrolases: a timely choice

Cellular and Molecular Life Sciences -     

Experientia majorum

Cellular and Molecular Life Sciences -     

DNA polymerases in prokaryotes and eukaryotes: Mode of action and biological implications

Cellular and Molecular Life Sciences -     

Meiotic chromosomes of the small indian lark (Alauda gulgula gulgula)

Cellular and Molecular Life Sciences -     

Temperature-induced hand inversion inBacillus subtilis macrofibers

Cellular and Molecular Life Sciences -     

Congressus

Cellular and Molecular Life Sciences -