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Books on the topic 'Tubulin'

Author: Grafiati

Published: 4 June 2021

Last updated: 10 March 2023

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1

service), SpringerLink (Online, ed. Tubulin-binding agents: Synthetic, structural and mechanistic insights. Berlin: Springer, 2009.

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2

Carlomagno, Teresa, ed. Tubulin-Binding Agents. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-69039-9.

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3

Yamauchi, Wei. Tubulin: Structure, functions, and roles in disease. Hauppauge, N.Y: Nova Science, 2011.

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4

Read, M. Tubulin in the erythrocytic stages of phasmodium falciparum. Manchester: UMIST, 1995.

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5

Leyland, Steven. A unique tubulin antiserum inhibits poleward chromosome movement in anaphase. Ottawa: National Library of Canada, 1990.

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6

Pape, Michaela. Charakterisierung des [beta]-Tubulin-Gens der kleinen Strongyliden des Pferdes. [S.l.]: [s.n.], 1999.

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7

Lamb, Jeremy Charles. Fluorescent derivatives of tubulin as probes for the analysis of microtubule dynamics. Norwich: University of East Anglia, 1985.

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8

Poetsch, Bettina. Zur Expression und Funktion von Aktin und Tubulin in der Photomorphogenese von Physarum polycephalum. Gauting bei München: Intemann, 1989.

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9

Kaluzienski, Mark Henry. Changes in rat skeletal muscle phenotype following colchicine disruption of motor axonal tubulin. Sudbury, Ont: Laurentian University, Behavioural Neuroscience Program, 1999.

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10

A, Cross R., and Kendrick-Jones J, eds. Motor proteins: A volume based on the EMBO Workshop, Cambridge, September 1990. Cambridge [England]: Company of Biologists, 1991.

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11

Jesús, Avila, ed. Microtubule proteins. Boca Raton, Fla: CRC Press, 1990.

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12

Paul, Grundy, Holgate Alan, Wong Bill, and International Symposium on Tubular Structures (6th : 1994 : Melbourne), eds. Tubular structures VI. Netherlands: A.A. Balkema, 1994.

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13

Kosteski, Nikola. Nailed tubular connections. Ottawa: National Library of Canada, 1996.

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14

Grundy, Paul, Alan Holgate, and Bill Wong. Tubular Structures VI. London: Routledge, 2021. http://dx.doi.org/10.1201/9780203735015.

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15

Farkas, József, and Károly Jármai. Tubular Structures VII. London: Routledge, 2022. http://dx.doi.org/10.1201/9780203735008.

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16

Farkas, József, and Károly Jármai. Tubular Structures VII. London: Routledge, 2022. http://dx.doi.org/10.1201/9780203735008.

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17

Andreyev, Sam. The tubular west. Toronto: Expert Press, 2003.

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18

Woods, Pamela. Tubular ribbon for florists. Stuttgart: Frech-Verlag, 1985.

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19

Totally tubular '80s toys. Iola, WI: Krause, 2010.

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20

Skolmen, Roar. Året på Tubuai. Oslo: Grøndahl, 1985.

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21

Amerio, Alberto, Pasquale Coratelli, and Shaul G. Massry, eds. Tubulo-Interstitial Nephropathies. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3892-9.

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22

Carlomagno, Teresa. Tubulin-Binding Agents: Synthetic, Structural and Mechanistic Insights. Springer Berlin / Heidelberg, 2014.

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23

Dunn, Cathy Savage. Genetic and molecular analysis of MEC-7, a -tubulin gene required for the production of 15-protofilament microtubules in the nematode Caenorhabditis elegans. [New York], 1992.

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24

Elliott, Elizabeth Margaret. The -tubulin gene family of Chinese hamster ovary cells. 1985.

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25

Tahir, Stephen Kenneth. Effect of high hydrostatic pressure on tubulin synthesis in deciliated "Tetrahymena". 1987.

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26

Freeman, Nancy Leigh. Sequence and expression of two alpha-tubulin genes from Mucor racemosus. 1992.

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27

Medina, John James. Molecular cloning and expression of the alpha and beta tubulin genes of Mucor racemosus. 1988.

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28

Motor proteins: A volume based on the EMBO Workshop, Cambridge, September 1990 (Journal of cell science). Company of Biologists, 1991.

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29

Mill, John Forbes. Regulation of tubulin gene expression by insulin, IGF-II, and NGF, in differentiating cloned human neuroblastoma cell line. 1986.

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30

Speeckaert, Marijn, and Joris Delanghe. Tubular function. Edited by Christopher G. Winearls. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0008.

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Assessment of tubular function is more complicated than the measurement of glomerular filtration rate. Different functions may be affecting according to the different segments of tubule involved. Key tests include concentrating and diluting capacity, and fractional excretion of sodium. Tubular proteinuria occurs when glomerular function is normal, but when the proximal tubules have a diminished capacity to reabsorb and to catabolize proteins, causing an increased urinary excretion of the low-molecular-mass proteins that normally pass through the glomerulus. Proximal tubular dysfunction is characterized by hypophosphataemia, and a variety of other abnormalities characteristics of the renal Fanconi syndrome. Distinguishing the location of the lesion in Renal Tubular Acidosis is considered in Chapter 35.

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31

Avila, Jesus. Microtubule Proteins. Taylor & Francis Group, 2018.

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32

Avila, Jesus. Microtubule Proteins. Taylor & Francis Group, 2018.

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33

Avila, Jesus. Microtubule Proteins. Taylor & Francis Group, 2018.

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34

Microtubule Proteins. Taylor & Francis Group, 2017.

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35

1937-, Brenner Barry M., and Stein Jay H. 1937-, eds. Modern techniques of ion transport. New York: Churchill Livingstone, 1987.

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36

C, Gonick Harvey, and Buckalew Vardaman M, eds. Renal tubular disorders: Pathophysiology, diagnosis, and management. New York: Dekker, 1985.

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37

Reader, Jocelyn, Sarah Lynam, Amy Harper, Gautam Rao, Maya Matheny, and Dana M. Roque. Ovarian Tumor Microenvironment and Innate Immune Recognition. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190248208.003.0004.

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Ovarian adenocarcinoma is typified by detection at late stages with dissemination of cancer cells into the peritoneal cavity and frequent acquisition of chemoresistance. A number of studies show the importance of the tumor microenvironment and innate immune recognition in tumor progression. Ovarian cancer cells can regulate the composition of their stroma to promote the formation of ascitic fluid rich in cytokines and bioactive lipids such as PGE2, and to stimulate the differentiation of stromal cells into a pro-tumoral phenotype. In response, cancer-associated fibroblasts, cancer-associated mesenchymal stem cells, tumor-associated macrophages, and other peritoneal cells can act through direct and indirect mechanisms to regulate tumor growth, chemoresistance via alteration of class III β‎ tubulin, angiogenesis and dissemination. This chapter deciphers the current knowledge about the role of stromal cells, associated secreted factors, and the immune system on tumor progression. This suggests that targeting the microenvironment holds great potential to improve the prognosis of patients with ovarian adenocarcinoma.

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38

Ellison, David H., and Arohan R. Subramanya. Clinical use of diuretics. Edited by Robert Unwin. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0033.

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Diuretics are widely employed to treat extracellular fluid volume expansion caused by heart failure, cirrhosis of the liver, nephrotic syndrome, and chronic kidney disease. Major classes of diuretic inhibit sodium reabsorption along the proximal tubule, the loop of Henle, the distal convoluted tubule, and the connecting and collecting tubules. Loop diuretics have the highest ceiling of action and often form the cornerstones of diuretic treatment of oedema. Members of this class are short-acting drugs, with different bioavailabilities, the specifics of which contribute importantly to a rational and effective approach to their use. They are not filtered substantially because they are all protein bound. They enter tubules by secretion along the proximal tubule, thereby gaining access to the Na-K-2Cl cotransporter of the thick ascending limb. Their dose–response curves are sigmoidal and altered by several disease processes. Chronic administration can elicit adaptive processes along the nephron that limit their efficacy. Distal convoluted tubule diuretics, such as the thiazides, inhibit NaCl absorption along the distal convoluted tubule. While used predominantly to treat hypertension, they are also useful to treat oedema, especially when combined with loop diuretics. Drugs acting along the connecting tubule and collecting duct either inhibit Na+ channels directly or block mineralocorticoid receptors. These drugs are effective in states of very high aldosterone secretion, and can also be used to reduce the hypokalaemia caused by other classes of diuretics. An evidence-based approach to treating the oedematous patient is described.

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39

Ortiz, Erica, Eric Ortiz, and Amos Ortiz. Tubular. Independently Published, 2016.

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40

Houillier, Pascal. Magnesium homeostasis. Edited by Robert Unwin. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0027.

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Magnesium is critically important in the process of energy release. Although most magnesium is stored outside the extracellular fluid compartment, the regulated concentration appears in blood. Urinary magnesium excretion can decrease rapidly to low values when magnesium entry rate into the extracellular fluid volume is low, which has several important implications: cell and bone magnesium do not play a major role in the defence of blood magnesium concentration; while a major role is played by the kidney and especially the renal tubule, which adapts to match the urinary magnesium excretion and net entry of magnesium into extracellular fluid. In the kidney, magnesium is reabsorbed in the proximal tubule, the thick ascending limb of the loop of Henle (TALH), and the distal convoluted tubule (DCT). Magnesium absorption is mainly paracellular in the proximal tubule and TALH, whereas it is transcellular in the DCT. The hormone(s) regulating renal magnesium transport and blood magnesium concentration are not fully understood. Renal tubular magnesium transport is altered by a number of hormones, mainly in the TALH and DCT. Parathyroid hormone, calcitonin, arginine vasopressin, ß-adrenergic agonists, and epidermal growth factor, all increase renal tubular magnesium reabsorption; in contrast, prostaglandin E2 decreases magnesium reabsorption. Non-hormonal factors also influence magnesium reabsorption: it is decreased by high blood concentrations of calcium and magnesium, probably via the action of divalent cations on the calcium-sensing receptor; metabolic acidosis decreases, and metabolic alkalosis increases, renal magnesium reabsorption.

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41

Bockenhauer, Detlef, and Robert Kleta. Approach to the patient with renal Fanconi syndrome, glycosuria, or aminoaciduria. Edited by Robert Unwin. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0041_update_001.

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Up to 80% of filtered salt and water is returned back into the circulation in the proximal tubule. Several solutes, such as phosphate, glucose, low-molecular weight proteins, and amino acids are exclusively reabsorbed in this segment, so their appearance in urine is a sign of proximal tubular dysfunction. An entire orchestra of specialized apical and basolateral transporters, as well as paracellular molecules, mediate this reabsorption. Defects in proximal tubular function can be isolated (e.g. isolated renal glycosuria, aminoacidurias, or hypophosphataemic rickets) or generalized. In the latter case it is called the Fanconi–Debre–de Toni syndrome, based on the initial clinical descriptions. However, in clinical practice it is usually referred to as just the ‘renal Fanconi syndrome’. Severity of proximal tubular dysfunction can vary, and may coexist with some degree of loss of glomerular filtration capacity. Causes include a wide range of insults to proximal tubular cells, including a number of genetic conditions, drugs and poisons.

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42

Davies, G., and M. G. Coutie. Tubular Structures. Taylor & Francis Group, 1993.

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43

Grundy. Tubular Structures. Taylor & Francis, 1994.

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44

Niemi, E. Tubular Structures. Routledge, 1990.

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45

Tubular Combustion. Momentum Press, 2013.

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46

Tubular Structures. Taylor & Francis Group, 1990.

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47

Dunn-Rankin, Derek, and Satoru Ishizuka. Tubular Combustion. Momentum Press, 2013.

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48

HUI, XU. tubular pump. Unknown, 1991.

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49

Herrington, William G., Aron Chakera, and Christopher A. O’Callaghan. Interstitial renal disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0160.

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Tubulointerstitial renal diseases affect the renal tubules and/or the supporting interstitial tissue around them. The glomeruli are typically spared in early disease. Acute interstitial nephritis is characterized by an inflammatory infiltrate (often containing eosinophils). Chronic tubulointerstitial nephritis (TIN) is characterized by extensive tubular atrophy and interstitial fibrosis. The processes are clinically distinct but a prolonged acute interstitial nephritis will develop into chronic disease. This chapter looks at the etiology of interstitial renal disease, as well as its symptoms and clinical features, demographics, complications, diagnosis, and treatment.

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50

Heidarpour, Amin, and Xiao-Ling Zhao, eds. Tubular Structures XVI. CRC Press, 2017. http://dx.doi.org/10.1201/9781351210843.

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