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Mechanisms regulating melanogenesis* - SciELO

The tumour microenvironment has been proposed to contribute to the increased genetic instability seen in cancer cells. Several studies have lent support to this notion, including a study that demonstrated a higher rate of genomic instability of mouse cells when grown in vivo as subcutaneous tumour implants in syngeneic mice, as measured using an EGFP reporter gene and a genomic minisatellite locus (Li et al., 2001). More specifically, hypoxia has been singled out as a major microenvironmental factor. Hypoxia, which appears to occur transiently within the tumour microenvironment, has been shown to lead to cycles of hypoxia and reoxygenation (Bindra and Glazer, 2005). This is thought to lead to DNA damage as a result of reactive oxygen species (ROS) and the enzyme superoxide dismutase. In addition to ROS leading to the formation of 8-oxoG, and accumulating evidence suggest a role for oxygen and ROS in causing single and (Bindra and Glazer, 2005). In addition to its ability to cause aberrations in DNA, these cycles of hypoxia and reoxygenation have been shown to affect DNA synthesis, by both interrupting this process and by leading to over-replication after reoxygenation (Bindra and Glazer, 2005; Cuvier et al., 1997; Young. and Hill, 1990; Young et al., 1990). Other studies have found that it is hypoxia induced gene amplification of p-Glycoprotein that is responsible for the observed resistance to adriamycin and doxorubicin (Luk et al., 1990; Rice et al., 1987), indicating that gene amplification may also be caused by hypoxia. Furthermore, emerging evidence suggests that hypoxia can influence the integrity of the genome by impacting upon DNA repair pathways. As described above, MLH1 is one of the key genes involved in mismatch repair. It was shown that hypoxia downregulates the expression of the MLH1 gene at the transcriptional level and this was thought to occur via chromatin remodeling, as treatment with an histone deacteylase inhibitor prevented the aforementioned decrease (Mihaylova et al., 2003). It has also been demonstrated that hypoxia enriches for MMR deficient cells (Hardman et al., 2001). Thus, DNA damage, defective DNA synthesis, gene amplification and the deregulation of DNA repair pathways all appear to be mechanisms by which hypoxia contributes to genetic instability. Little is still known about other microenvironmental factors that may lead to instability. However, it has been suggested that the tumour microenvironment may represent in mammalian cells a conserved evolutionary mechanism that increases the rate of mutation in response to cellular stresses, which preferentially gives cancer cells a survival advantage (Bindra and Glazer, 2005).

Genetics is the study of genes, genetic variation, and heredity in living organisms

AB - Mammalian cells use an exquisitely sensitive mechanism to control the amount of cholesterol and fatty acids in their membranes. This process relies on a feedback system that adjusts the rates of transcription of genes encoding the low density lipoprotein receptor and multiple enzymes in the cholesterol and fatty acid biosynthetic pathways. When cellular cholesterol levels are depleted, these genes are all transcribed in abundant amounts, and their transcription is repressed when sterols build up within the cell. Until recently, the mechanism of this regulation was elusive. How do cells sense the level of a membrane-embedded lipid such as cholesterol and how is this information transmitted to the nucleus where gene transcription is regulated? Answers are now beginning to emerge from the study of a newly discovered family of transcription-regulating proteins called sterol regulatory element binding proteins.

Anais Brasileiros de Dermatologia Print version ISSN 0365-0596 An

Genetic Mechanisms Underlying Apimaysin and Maysin Synthesis and Corn Earworm Antibiosis in Maize (Zea mays L.)

N2 - Mammalian cells use an exquisitely sensitive mechanism to control the amount of cholesterol and fatty acids in their membranes. This process relies on a feedback system that adjusts the rates of transcription of genes encoding the low density lipoprotein receptor and multiple enzymes in the cholesterol and fatty acid biosynthetic pathways. When cellular cholesterol levels are depleted, these genes are all transcribed in abundant amounts, and their transcription is repressed when sterols build up within the cell. Until recently, the mechanism of this regulation was elusive. How do cells sense the level of a membrane-embedded lipid such as cholesterol and how is this information transmitted to the nucleus where gene transcription is regulated? Answers are now beginning to emerge from the study of a newly discovered family of transcription-regulating proteins called sterol regulatory element binding proteins.

AB - This chapter discusses the mechanisms regulating the synthesis of bacterial membrane lipid. The regulation of synthesis of membrane lipid can be achieved by (1) control of membrane phospholipid acyl-group composition and (2) regulation of the rate of phospholipid synthesis. Major progress on the sn-glycerol-3-phosphate acyltransferase is permitted by genetic cloning and by synthesis of native acyl-ACP substrates. A similar combination of genetic and biochemical approaches has led to a detailed knowledge of the mechanism of temperature control. β-ketoacyl-ACP synthase II is required for temperature control. This enzyme is not involved in isothermal control. β-ketoacyl-ACP synthase II therefore seems tailored for its role in temperature regulation, and temperature control seems to be superimposed on the normal (isothermal) regulatory mechanism. E. coli developed temperature control by evolving a temperature-sensitive isozyme to catalyze the synthesis of the required unsaturated fatty acid. Although simple regulatory mechanisms such as that of temperature control explains the phenomenology of the regulation of bacterial lipid synthesis, the regulation of phospholipid synthesis by the relA gene may be an exception. The unreliable nature of results obtained in vitro means that sophisticated approaches must be developed to ascertain the physiological relevance of ppGpp inhibition of a given enzyme.

vol.88 no.1 Rio de Janeiro Jan./Feb

BioCoach Activity Concept 6: The Transcription Process

The fungal cell wall is an essential structure which protects cells from various environmental stresses such as hyper- or hypo-osmosis, and endows them with specific morphology in response to their life or cell division cycle. In addition, the cell wall has a variety of enzymatic activities per se, which are required for nutritional uptake, secretion, and cell adhesion including mating processes. In addition to these cytological interests, clinical demands to clarify the regulatory mechanisms of cell wall synthesis have been increasing, since the cell wall is a unique and effective target of antifungal agents. However, the molecular mechanisms are poorly understood at present, although the role of several signal transduction pathways have recently been implicated in regulation. In this review, the author focuses on genes and their interactions which are involved in fission yeast cell wall biogenesis.

Our group has observed that Bik is a critical factorfor resistance to tamoxifen, and utilizing MCF-7 cells hasdemonstrated that BIK mRNA and protein were strongly induced byestrogen-starvation or anti-estrogen treatment (,). Conversely, knockdown of BIK bysiRNA significantly inhibited the apoptosis caused by tamoxifentreatment, finding low expression of BAX, BAK and PUMApro-apoptotic proteins and high expression of some anti-apoptoticproteins, such as BCL-2 and MCL-1 in BIK siRNA-transfected cellsafter treatment with TAM (,).These data demonstrated that Bik is an important factor in theTAM-induced apoptosis process, which may regulate mitochondrialintegrity by modulation of pro- and anti-apoptotic proteins. Ourresults showed that suppression of the gene exhibitedanti-apoptotic effects in TAM-treated MCF-7 cells. These data maybe useful for future studies to establish the mechanisms ofregulation of TAM resistance in breast cancer. In women with thisneoplasm and with positive ER, it may be important to determine BIKprotein levels to define whether or not TAM is the appropriatetreatment (). A possiblemechanism of resistance to apoptosis has been established and hasbeen described using mouse fibroblasts transformed with v-src as amodel. This group demonstrated that Src-dependent resistance tocell death relies on Src ability to inhibit the mitochondrialpathway of apoptosis by specifically increasing the degradationrate of the BH3-only protein Bik by proteasome due to thephosphorylation of Bik. This effect relies on the activation of theRas-Raf-Mek1/2-Erk1/2 pathway and on the phosphorylation of Bik onThr124, driving Bik ubiquitylation on Lys33 and subsequentdegradation by the proteasome. These results suggest that Bik couldbe a rate-limiting factor for apoptosis induction of tumor cellsexhibiting deregulated Erk1/2 signaling, which may provide newopportunities for cancer therapies ().

Sheron Perera, BSc and Bharati Bapat, PhD
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Bile Acid Synthesis and Utilization

When in the timeline of events leading to metabolic disease do sphingolipids accumulate? What regulatory mechanisms govern rates of ceramide synthesis or degradation?

The end products of cholesterol utilization are the bile acids

This chapter discusses the mechanisms regulating the synthesis of bacterial membrane lipid. The regulation of synthesis of membrane lipid can be achieved by (1) control of membrane phospholipid acyl-group composition and (2) regulation of the rate of phospholipid synthesis. Major progress on the sn-glycerol-3-phosphate acyltransferase is permitted by genetic cloning and by synthesis of native acyl-ACP substrates. A similar combination of genetic and biochemical approaches has led to a detailed knowledge of the mechanism of temperature control. β-ketoacyl-ACP synthase II is required for temperature control. This enzyme is not involved in isothermal control. β-ketoacyl-ACP synthase II therefore seems tailored for its role in temperature regulation, and temperature control seems to be superimposed on the normal (isothermal) regulatory mechanism. E. coli developed temperature control by evolving a temperature-sensitive isozyme to catalyze the synthesis of the required unsaturated fatty acid. Although simple regulatory mechanisms such as that of temperature control explains the phenomenology of the regulation of bacterial lipid synthesis, the regulation of phospholipid synthesis by the relA gene may be an exception. The unreliable nature of results obtained in vitro means that sophisticated approaches must be developed to ascertain the physiological relevance of ppGpp inhibition of a given enzyme.

Normal Plasma Cholesterol in an 88-Year-Old Man Who …

Mammalian cells use an exquisitely sensitive mechanism to control the amount of cholesterol and fatty acids in their membranes. This process relies on a feedback system that adjusts the rates of transcription of genes encoding the low density lipoprotein receptor and multiple enzymes in the cholesterol and fatty acid biosynthetic pathways. When cellular cholesterol levels are depleted, these genes are all transcribed in abundant amounts, and their transcription is repressed when sterols build up within the cell. Until recently, the mechanism of this regulation was elusive. How do cells sense the level of a membrane-embedded lipid such as cholesterol and how is this information transmitted to the nucleus where gene transcription is regulated? Answers are now beginning to emerge from the study of a newly discovered family of transcription-regulating proteins called sterol regulatory element binding proteins.

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