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Introduction
Published in James F. Kane, Multifunctional Proteins: Catalytic/Structural and Regulatory, 2019
Thirdly, Chou et al.62 reported on a self-regulating repressor from the Tn3 element. Their results suggest that this regulatory protein not only controls its own synthesis, but represses translocation of the element from one carrier to another. It has not been established, however, that this repressor protein contains discrete domains.
Role of Nonhistone Chromosomal Proteins in Selective Gene Expression
Published in Gerald M. Kolodny, Eukaryotic Gene Regulation, 2018
I.R. Phillips, E.A. Shephard, J.L. Stein, G.S. Stein
The question which, therefore, arises is how specific regions of the genome are rendered transcribable — or how genes are “turned on” and “turned off”. In microbial systems, significant inroads have been made toward understanding the mechanism by which genes are regulated. Specific repressor proteins have been isolated which interact with defined genetic sequences and render genes nontranscribable.1,2 Specific activators have been shown to modify the interactions of these repressors with DNA and, hence, permit transcription.3,4 The two prokaryotic systems which have been most extensively characterized are the lac operon5 and the bacteriophage lambda.6 While our understanding of prokaryotic gene regulation has progressed to a sophisticated level, caution must be exercised in assuming that analogous mechanisms are operative in eukaryotic cells.
Kinetic Thinking: Back to the Future
Published in Clive R. Bagshaw, Biomolecular Kinetics, 2017
Making progress by 1D diffusion requires a large n value, and hence, kslide must be very much greater than koff for the repressor to remain attached. The root-mean-squared distance travelled is proportional to because passive diffusion provides no directionality. A 1D search by passive diffusion becomes slow in finding a target that is hundreds of base pairs away from the initial nonspecific encounter site (cf. Table 3.1). Indeed, nonspecific binding sites become inhibitory when separated by a large distance from the target site. To make progress, the repressor protein must dissociate and rebind elsewhere. Here, we need to consider the persistence length of DNA of 50 nm (150 bp), which indicates that in vitro, DNA containing thousands of base pairs will be a random coil with an approximately spherical boundary. Once the repressor proteins enters the space occupied by the DNA coil, there is a high probability that, following a dissociation event, it will bind to another region of the same DNA molecule rather than escaping back into bulk solvent. Protein rebinding further along a linear DNA segment is termed “hopping,” while movement between loops within the DNA coil is termed “jumping.” Translocation to another region of the DNA may also be achieved by DNA bending to such an extent that a new segment comes into contact with the bound protein, which relocates by intersegment transfer (Figure 10.3).
An inflammatory triangle in Sarcoidosis: PPAR-γ, immune microenvironment, and inflammation
Published in Expert Opinion on Biological Therapy, 2021
Parnia Jabbari, Mona Sadeghalvad, Nima Rezaei
Upon ligand binding, PPARs form a heterodimer with retinoid x receptors (RXRs) to identify and bind to PPAR response elements (PPRE) in the promoter of target genes. PPRE consists of two direct repeats ‘AGGTCA’ separated by a single nucleotide named DR-1 element. Same as the other nuclear hormone receptors, the function of PPARs could be influenced by the interaction with co-repressor or co-activator proteins. In the inactivated-state or absence of the ligand, PPARs interact with the co-repressor proteins that lead to inhibiting the transcription of target genes. Upon activation of PPARs, co-repressors are dissociated and co-activators including steroid receptor co-activator-1 (SRC-1) and PPAR ligand-protein are recruited to the promoter site of target genes that lead to initiation of transcription [41].
Valproic acid attenuates CCR2-dependent tumor infiltration of monocytic myeloid-derived suppressor cells, limiting tumor progression
Published in OncoImmunology, 2020
Zhiqi Xie, Tamami Ikegami, Yukio Ago, Naoki Okada, Masashi Tachibana
It has been well established that gene expression can be modulated by chromatin remodeling.33 Although histone acetylation usually increases gene transcription, previous research has also shown that in some cases histone acetylation can suppress gene transcription.34 In our study, down-regulation of CCR2 expression could be correlated with the acetylation status of histone. Hence, direct activation of a CCR2 repressor protein through its acetylation may result in down-regulation of CCR2 expression. Alternatively, previous studies have shown that VPA has the ability to induce apoptosis in a number of different cell types, including tumor cells and immune cells, by regulating apoptosis related genes through HDAC inhibition.35,36 Thus, the possibility that VPA is more cytotoxic to CCR2+ M-MDSCs still remains, and further research is warranted. On the other hand, although CCR2 expression on the TAMs also decreased slightly, there were no significant changes in TAMs found in the tumor site. In addition to the CCL2/CCR2 axis, several other tumor derived factors attract circulating monocytes to the tumor site and differentiate into TAMs, such as chemokines CSF1, CCL5, CXCL12, and CX3CL1.37 VPA might up-regulate these factors, resulting in no significant change in the levels of TAMs at the tumor site.
The impact of cigarette smoking on protamines 1 and 2 transcripts in human spermatozoa
Published in Human Fertility, 2019
Mohammed Hamad, Nyaz Shelko, Mathias Montenarh, Mohammed Eid Hammadeh
Regulation of the translation of protamines starts with processing RNA through intron splicing and polyadenylation of mRNA (Steger, 1999). The mRNA’s polyadenylation tail is crucial for binding translation repressor proteins and prevents the degradation of mRNA in the cytosol. Storing mRNA in messenger ribonucleoprotein particles (mRNP) (Schmidt, Hanson, & Capecchi, 1999) and binding to specific translation repressor proteins that attach to the poly-A, the 5′-UTR and the 3′-UTR sequences of mRNA stop translation (Aoki & Carrell, 2003). During the spermatid elongation stage, translation suppression is removed by: (i) covalent modification of the mRNP, (ii) discharge of translatable mRNA and (iii) removing the translation repressor proteins. These events will make the poly-A tail of the mRNA shorter by a partial deadenylation (Domenjoud, Kremling, Burfeind, Maier, & Engel, 1991).