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Books on the topic 'Steroid biosynthesis'

Author: Grafiati

Published: 4 June 2021

Last updated: 3 February 2022

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1

Figueiredo, Carlos Amada, and Luiza Cação Garces. Steroids: Biosynthesis, functions, and health implications. New York: Nova biomedical/Nova Science Publishers, Inc., 2012.

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2

Kato, T., W. Krämer, K. H. Kuck, D. M. Norris, and H. Scheinpflug, eds. Sterol Biosynthesis Inhibitors and Anti-Feeding Compounds. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-69790-6.

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3

I, Mason J., ed. Genetics of steroid biosynthesis and function. London: Taylor & Francis, 2002.

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4

Mason, J. I. Genetics of Steroid Biosynthesis and Function (Moderngenetics). CRC, 2002.

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5

Rižner, Tea Lanišnik, Walter Jäger, and Csilla Özvegy-Laczka, eds. Relevance of Steroid Biosynthesis, Metabolism and Transport in Pathophysiology and Drug Discovery. Frontiers Media SA, 2019. http://dx.doi.org/10.3389/978-2-88945-887-5.

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6

Patisaul, Heather B., and Scott M. Belcher. Receptor and Enzyme Mechanisms as Targets for Endocrine Disruptors. Oxford University Press, 2017. http://dx.doi.org/10.1093/acprof:oso/9780199935734.003.0005.

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In this chapter, the current understanding of the mechanisms of endocrine disruption on the brain and nervous system are presented. Because the overwhelming majority of mechanistic studies on EDCs have focused on the actions mediated by nuclear hormone receptors, this mechanisms is described in detail. The chapter also discusses the classic transcriptional mechanisms of steroid action and the impact of EDCs on rapid signaling (non-genomic) mechanisms. It presents an overview of the enzymes and pathways involved in the biosynthesis of steroid hormones, which are critical to proper functioning of the HPA and HPG axis, and the neuroactive steroids synthesized and active in the mammalian brain. The potential for EDCs to alter metabolic enzymes, with a focus on possible targets in the metabolic blood-brain barrier, is presented as a potential, though largely unexplored, mode of EDC action in the brain.

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7

Sarphare, Geeta, Ryan Lee, and Elaine Tierney. Smith-Lemli-Opitz Syndrome and Role of Cholesterol in Autism. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199744312.003.0012.

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Cholesterol is manufactured throughout the body, but predominantly in the liver, and is essential for many metabolic processes. Cholesterol plays a critical role in forming membranes and myelin sheaths and is a precursor molecule for the synthesis of steroid hormones, neuroactive steroids, oxysterols, and vitamin D. It is also essential in the production of bile acids, which in turn helps the body absorb cholesterol and fat-soluble vitamins. Cholesterol is essential in embryonic and fetal development and is also critical in regulating lipid raft processes such as signaling and trafficking (Korade & Kenworthy, 2008). Cholesterol biosynthesis begins with the formation of squalene and ends with the reduction of 7-dehydrocholesterol (7DHC) into cholesterol by the enzyme 7DHC reductase, and then its spontaneous isomer, 8-dehydrocholesterol (8DHC). Smith-Lemli-Opitz syndrome (SLOS, Mendelian Inheritance in Man #270400) is an autosomal recessive disorder due to an inborn error of cholesterol biosynthesis (Elias et al., 1993; Irons, Elias, Salen, Tint, & Batta, 1993; Tint et al., 1994). Smith-Lemli-Opitz syndrome has an estimated incidence among individuals of European ancestry in Canada and the United States of 1 in 15,000 to 1 in 60,000 births (Bzdúch, Behulova, & Skodova, 2000; Lowry & Yong, 1980; Opitz, 1999; Ryan, Bartlett, Clayton, Eaton, Mills, Donnai, & Burn, 1998) and a carrier frequency of 1 in 30 to 1 in 50 (Nowaczyk & Waye, 2001).

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8

1949-, Berg D., and Plempel M. 1930-, eds. Sterol biosynthesis inhibitors: Pharmaceutical and agrochemical aspects. Chichester, Eng: Ellis Horwood, 1988.

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9

1946-, Kato T., ed. Sterol biosynthesis inhibitors and anti-feeding compounds. Berlin: Springer-Verlag, 1986.

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10

(Editor), M. Plempel, ed. Sterol Biosynthesis Inhibitors: Pharmaceutical and Agrochemical Aspects (Ellis Harwood Series in Biomedicine). Vch Pub, 1988.

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11

Morrow, Gary W. Bioorganic Synthesis. Oxford University Press, 2016. http://dx.doi.org/10.1093/oso/9780199860531.001.0001.

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Building on the foundation of a one-year introductory course in organic chemistry, Bioorganic Synthesis: An Introduction focuses on organic reactions involved in the biosynthesis of naturally-occurring organic compounds with special emphasis on natural products of pharmacological interest. The book is designed specifically for undergraduate students, rather than as an exhaustive reference work for graduate students or professional researchers and is intended to support undergraduate courses for students majoring in chemistry, biochemistry, biology, pre-medicine, and bioengineering programs who would benefit from a deeper understanding of the chemical logic of reactions carried out in organisms and the origins and uses of the important organic compounds they often produce. The book assumes no prior background in biochemistry and consists of eight chapters: i) a brief review of relevant topics from introductory organic chemistry; ii) presentation of essential organic and biochemical reactions used throughout the book along with a brief introduction to coenzymes; iii) review of basic carbohydrates and the biosynthesis of amino acids; iv) the terpenoid pathway for biosynthesis of all important classes of terpenoids and steroids; v) the acetate pathway for biosynthesis of saturated and unsaturated fatty acids, prostaglandins and acetate-derived polyketide natural products; vi) the biosynthesis of the shikimate pathway products derived from aromatic amino acids; vii) an introduction to biosynthesis of major alkaloids and related nitrogenous compounds; and viii) an overview of laboratory organic synthesis as it relates to the challenges faced by synthetic and medicinal chemists who must recreate intricate natural product structures in the laboratory.

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12

1938-, Desjardins Claude, Serono Symposia USA, and Testis Workshop on Cellular and Molecular Regulation of Testicular Cells (13th : 1995 : Raleigh, N.C.), eds. Cellular and molecular regulation of testicular cells. New York: Springer, 1996.

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13

Gluckman, Sir Peter, Mark Hanson, Chong Yap Seng, and Anne Bardsley. Vitamin B3 (niacin) in pregnancy and breastfeeding. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198722700.003.0009.

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Niacin (as nicotinamide) is a component of coenzyme systems that function in the reductive biosynthesis of fatty acids and steroids, including cholesterol, and are involved in cell signalling. Niacin deficiency is rare, as the daily requirement can usually be met by food sources, and also via synthesis from tryptophan, which is present in dietary proteins. The prevalence of niacin deficiency is higher in populations consuming mainly corn or sorghum as a dietary staple. Corn contains niacin, but only in a bound form that is nutritionally unavailable. The additional needs for niacin during pregnancy are mirrored by the increased energy intake needs, and dietary supplementation is only necessary in cases of overall poor nutritional intake.

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14

Frenkel, Joost, and Hans R. Waterham. Mevalonate Kinase Deficiency. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0039.

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Mevalonate kinase deficiency (MKD) is an autosomal recessive inborn error of isoprenoid biosynthesis, a pathway yielding sterols and nonsterol isoprenoids.In patients, the enzyme activity of mevalonate kinase is severely reduced due to mutations in the encoding gene, MVK. The substrate, mevalonate, accumulates and is elevated in blood and urine. Shortage of certain downstream products of the pathway, nonsterol isoprenoids, leads to dysregulation of the innate immune system, activation of inflammasomes, and interleukin (IL)-1 mediated inflammation.Symptoms start in early childhood with recurrent attacks of fever, vomiting, diarrhea, headache, sore throat, abdominal pain, arthralgias, painful lymphadenopathy, hepatosplenomegaly, skin rash, and mucosal ulcers. Severely affected patients have additional symptoms, such as intellectual impairment, progressive cerebellar ataxia, and tapetoretinal degeneration. Complications include intestinal obstruction, AA-amyloidosis, hemophagocytosis, and severe infection.Management of MKD is directed at controlling inflammation.

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15

1951-, Taylor Peter G., Royal Society of Chemistry (Great Britain), and Open University, eds. Mechanism and synthesis. Cambridge: Royal Society of Chemistry, 2002.

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16

Taylor, P. G. Mechanism and Synthesis. Royal Society of Chemistry, 2002.

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