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Relevant bibliographies by topics / Cell surface molecules][Morphogenesis / Books

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Books on the topic 'Cell surface molecules][Morphogenesis'

Author: Grafiati

Published: 4 June 2021

Last updated: 11 February 2022

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Consult the top 16 books for your research on the topic 'Cell surface molecules][Morphogenesis.'

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1

Chattopadhyay, Kausik, and Subhash C. Basu, eds. Biochemical and Biophysical Roles of Cell Surface Molecules. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-13-3065-0.

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2

Surface and interfacial aspects of cell adhesion. Leiden: Boston, 2010.

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3

The cell surface in embryogenesis and carcinogenesis. Caldwell, N.J: Telford Press, 1989.

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4

Cole, Louise. Immunocytochemical studies of fungal cell surface molecules and the vicia faba-Botrytis interaction. Oxford: Oxford Brookes University, 1996.

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5

Michaela, Kendall, Rehfeldt Florian, and SpringerLink (Online service), eds. Adhesion of Cells, Viruses and Nanoparticles. Dordrecht: Springer Science+Business Media B.V., 2011.

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6

Malcolm, Steinberg, ed. The Cell surface in development and cancer. New York: Plenum Press, 1986.

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7

Biochemical and Biophysical Roles of Cell Surface Molecules. Springer, 2019.

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8

Developmental Biology:A Comprehensive Synthesis: Volume 3: The Cell Surface in Development and Cancer (Developmental Biology). Springer, 1986.

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9

Yamagata, Masahito, and Hiroko Bannai, eds. Neuroscience and Neurotechnology of Neuronal Cell Surface Molecules in Neural Circuits. Frontiers Media SA, 2021. http://dx.doi.org/10.3389/978-2-88971-149-9.

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10

Lieping, Chen, ed. The B7-CD28 family molecules. Georgetown, Tex: Landes Bioscience/Eurekah.com, 2003.

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11

Chen, Lieping. The B7-CD28 Family Molecules. Springer US, 2010.

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12

Neural Surface Antigens: From Basic Biology Towards Biomedical Applications. Elsevier Science & Technology Books, 2015.

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13

Hong, Claire. Mapping the distribution of cell surface molecules by chromophore localization in the transmission electron microscope via low electron energy loss imaging. 2004.

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14

Colbert, Robert A., and Paul Bowness. Immune mechanisms: HLA-B27. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198734444.003.0006.

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HLA-B27 is present in the majority of patients with ankylosing spondylitis (AS). Although we have learned a considerable amount about the natural immunologic function of HLA class I proteins, this has not provided a definitive mechanism of AS pathogenesis. While HLA-B27 is adept at presenting antigenic peptides to CD8+ T cells, ‘arthritogenic’ peptides targeted by a cross-reactive T or natural killer cell response have not been described, nor have autoreactive T cells been found. Newer concepts have evolved based on the propensity of HLA-B27 to ‘misbehave’, both inside cells and on the cell surface. Misfolded HLA-B27 molecules may stimulate an endoplasmic reticulum stress response, promoting production of IL-23 and then IL-17 and related cytokines. Aberrant cell-surface HLA-B27 molecules are ligands for natural killer and related immunoreceptors, and recognition can lead to IL-17 proinflammatory responses. There is growing evidence to suggest that these aberrant behaviours contribute to AS pathogenesis.

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15

Woywodt, Alexander, and Diana Chiu. Drug-induced and toxic glomerulopathies. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0082.

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Glomerulopathies induced by particular exogenous compounds or molecules include those attributable to toxicity, and those caused by inducing an immune or autoimmune response. Tubules are more commonly the target of toxicity as they absorb and concentrate components of filtrate. Damage to endothelial cells may account for thrombotic microangiopathy in response to calcineurin inhibitors. Endothelial cells are also likely to be the target in drug-induced small vessel vasculitis. Toxicity to podocytes accounts for focal segmental glomerulosclerosis caused by pamidronate and other agents. Chloroquine can cause a remarkable pseudo-storage disorder with inclusions in podocytes that resemble those seen in Fabry disease. The mechanism by which drugs cause minimal change disease, another podocyte disorder, is not known. Membranous nephropathy may be caused by exposure to gold, mercury, and some other drugs; this is antibody mediated and presumably the targets are altered podocyte surface molecules. Inhibitors of the mammalian target of rapamycin (mTOR) cause proteinuria, possibly through effects on vascular endothelial growth factor, inhibitors of which are associated with not only proteinuria (an expected podocyte effect) but also thrombotic microangiopathy (endothelial cell effect). This latter may be through disturbing podocyte-endothelium cross-signaling.

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16

Cattran, Daniel C., and Heather N. Reich. Membranous glomerulonephritis. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0064_update_001.

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It has been clear for several decades from comparison with the rodent model disease Heymann nephritis that membranous glomerulonephritis (MGN) is an immune condition in which antibodies, usually autoantibodies, bind to targets on the surface of podocytes. However, the antigen in Heymann nephritis, megalin, is not present on human podocytes. The first potential antigen was identified by studying rare examples of maternal alloimmunization, leading to congenital membranous nephropathy in the infant caused by antibodies to neutral endopeptidase. More recently, the target of autoantibody formation in most patients with primary MGN has been identified to be the phospholipase A2 receptor, PLA2R. Genome-wide association studies identify predisposing genetic loci at HLADQ and at the locus encoding the autoantigen itself. So antibodies to at least two different molecular targets can cause MGN, and it seems likely that there may be other targets in secondary types of MGN, and possibly haptenized or otherwise modified molecules are implicated in drug- and toxin-induced MGN. Once antibodies are fixed, animal models and human observations suggest that complement is involved in mediating tissue damage. However, immunoglobulin G4, not thought to fix complement, is the predominant isotype in human MGN, and the mechanisms are not fully unravelled. Podocyte injury is known to cause proteinuria. In MGN, antibody fixation or cell damage may stimulate production of extracellular matrix to account for the increased GBM thickness with ‘podocyte type’ basement membrane collagen isoforms, and ultimately cell death and glomerulosclerosis.

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