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Genetic Regulation of Principal Microorganisms (Yeast, Zymomonas mobilis, and Clostridium thermocellum) Producing Bioethanol/Biofuel
Published in Ayerim Y. Hernández Almanza, Nagamani Balagurusamy, Héctor Ruiz Leza, Cristóbal N. Aguilar, Bioethanol, 2023
Dania Sandoval-Nuñez, Teresa Romero-Gutiérrez, Melchor Arellano-Plaza, Anne Gschaedler, Lorena Amaya-Delgado
In the process of regulating gene expression, the participation of expression modulating sequences plays a very important role. These sequences can intensify or silence the transcription process. Enhancers are sequences that stimulate transcription and whose location can be thousands of nucleotides away from the promoter. Silencers are sequences that inhibit transcription and can also be located far away from the promoter. For K. marxianus, few activating or repressor proteins have been reported that interact with enhancer sequences or silencers. For example, Spt15 is a protein that intensifies ethanol yields [66]. In contrast, the participation of TFs such as HSF1 and MSN2 confers resistance to chemicals such as furfural, phenol, and acetic acid and increases lignocellulosic ethanol production [60].
Use of Recombinant DNA Technology for Engineering Mammalian Cells to Produce Proteins
Published in Anthony S. Lubiniecki, Large-Scale Mammalian Cell Culture Technology, 2018
The transcriptional enhancer appears to be a primary regulator of transcriptional activity. Some enhancers located in viruses, e.g., polyoma (88) or Moloney murine sarcoma virus (89), show a host cell preference and thus contribute to the host range of the virus. Others, like the SV40 enhancer (90), the Rous sarcoma virus (RSV) LTR (91), and the human cytomegalovirus (CMV) enhancer (92), are very active in a wide variety of cell types from many species. Enhancers with strict cell type specificity have been observed in many cellular genes, most notably the immunoglobulin genes (93-95) and the insulin gene (96), and are likely primary cis-acting determinants in tissue specificity of gene transcription. The addition of a strong enhancer can increase transcriptional activity by 10- to 100-fold. Thus, most expression vectors include a strong enhancer, frequently derived from SV40, RSV, or CMV.
Cell Line Development
Published in Wei-Shou Hu, Cell Culture Bioprocess Engineering, 2020
In addition to the strength of the promoter, other elements affect the transcript level of the GOI. The human CMV, in the presence of intron A, has been shown to enhance the protein expression levels of the GOI.12 By including the 5′ and 3′ flanking control regions of EF-1α, the expression of the GOI driven by CMV or the human EF-1α promoter in CHO cells can be increased.13 Enhancers are DNA sequences that increase gene transcription and may not necessarily be located close to the promoter sequence. In some cases, a promoter such as CMV is used in conjunction with its associated enhancer sequences in the vector construct.
Inhibitory effect of particulate matter on toll-like receptor 9 stimulated dendritic cells by downregulating mitogen-activated protein kinase and NF-κB pathway
Published in Journal of Toxicology and Environmental Health, Part A, 2020
Madeeha Arooj, Irshad Ali, Hee Kyoung Kang, Jin Won Hyun, Young-Sang Koh
Innate immune cells such as dendritic cells (DCs) and macrophages are key endogenous components to counteract pathogens and serve as a link between innate and adaptive immunity. Antigen-presenting cells (APCs) recognize pathogen-associated molecular patterns (PAMPs) through pattern recognition receptors (PRRs) (Akira and Takeda 2004; Koo et al. 2012). Toll-like receptors (TLRs) interaction with PAMPs activates major signal transduction pathways including mitogen-activated protein kinase (MAPK) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and induces cytokine production which serves as a trigger to initiate T-cell-mediated immunity (Akira and Takeda 2004). MAPKs including extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38 kinase play a key role in apoptosis, cell survival, proliferation, differentiation, and inflammation. NF-κB is a rapid-acting transcription factor that aids in the expression of cytokines and cell survival. Under quiescent conditions, NF-κB, a transcription factor within cytosol is coupled with specific inhibitor nuclear factor of kappa light polypeptide gene enhancer in B-cells, alpha (IκBα). Upon TLR stimulation, IκBα is phosphorylated and ubiquitinated, which leads to proteasomal degradation and translocation of NF-κB into the nucleus where it regulates transcription of various inflammatory genes including cytokines (Akira and Takeda 2004; Blasius and Beutler 2010; Koo et al. 2012).
Biochanin A prevents 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced adipocyte dysfunction in cultured 3T3-L1 cells
Published in Journal of Environmental Science and Health, Part A, 2019
Eun Mi Choi, Kwang Sik Suh, So Young Park, Sang Ouk Chin, Sang Youl Rhee, Suk Chon
The process of adipocyte differentiation is influenced by various extrinsic factors and intracellular signaling pathways.[23] [Ca2+]i modulates adipocyte lipid metabolism and inhibits the early stages of murine adipogenesis.[24] Neal and Clipstone[25] reported that calcineurin mediates Ca2+-dependent inhibition of adipocyte differentiation in 3T3-L1 cells by preventing expression of the proadipogenic transcription factors PPARγ and CCAAT-enhancer binding protein-a (C/EBP)/enhancer binding protein-α. TCDD rapidly increases the concentration of [Ca2+]i through a non-genomic pathway.[26,27] The increase in [Ca2+]i activates enzymes and transcriptional factors.[28] Furthermore, the action of TCDD is clearly blocked by several calcium signaling blockers,[29] suggesting that the effect of TCDD is mediated by calcium-triggered activation of downstream genes. In the present study, biochanin A reduced the TCDD-induced increase in [Ca2+]i. Therefore, biochanin A increases adipocyte differentiation in the presence of TCDD by reducing [Ca2+]i.
Discovery of genetic risk factors for disease
Published in Journal of the Royal Society of New Zealand, 2018
In 1999 I moved to the Queensland Institute for Medical Research (QIMR) to lead a molecular genetics laboratory within a group studying genetic contributions to human traits and diseases. The Brisbane group had many years’ experience working with twin families to estimate genetic contributions for many conditions. We embarked on a significant programme to collect biological samples from twin families and disease cohorts for mapping studies. Risk factors for melanoma include genes associated with mole count and pigmentation. While linkage studies lack power to detect genetic risk factors for most complex human traits and diseases, some genes affecting pigmentation have sufficiently large effects that the location of these genes can be detected. Using linkage mapping, we mapped the major locus for blue/brown eye colour to chromosome 15 in the region of the oculocutaneous albinism II (OCA2) gene (Zhu et al. 2004). Subsequent fine mapping studies identified a single SNP (rs12913832) which accounted for 95% of the variation in blue/brown eye colour (Sturm et al. 2008). This SNP is located 21 kb upstream of OCA2 within an intron of the adjacent gene, HECT and RLD domain containing E3 ubiquitin protein ligase 2 (HERC2), in an enhancer regulating OCA2 transcription (Visser et al. 2012). The allele for blue eyes reduces the recruitment of transcription factors helicase-like transcription factor (HLTF), lymphoid enhancer-binding factor 1 (LEF1), and melanogenesis associated transcription factor (MITF), and reduces interactions between the enhancer and the promoter of OCA2 (Visser et al. 2012).