Search results for: Transcription




The MYBL1/TCFL5 transcription network: two collaborative factors with central role in male meiosis.
Male gametogenesis, spermatogenesis, is a stepwise developmental process to generate mature sperm. The most intricate process of spermatogenesis is meiosis during which two successive cell divisions ensue with dramatic cellular and molecular changes to produce haploid cells. After entry into meiosis, several forms of regulatory events control the orderly progression of meiosis and the timely entry into post-meiotic sperm differentiation. Among other mechanisms, changes to gene expression are controlled by key transcription factors. In this review, we will discuss the gene regulatory mechanisms underlying meiotic entry, meiotic progression, and post-meiotic differentiation with a particular emphasis on the MYBL1/TCFL5 regulatory architecture and how this architecture involves in various forms of transcription network motifs to regulate gene expression.Martin Säflund, Deniz M Özata
1612 related Products with: The MYBL1/TCFL5 transcription network: two collaborative factors with central role in male meiosis.
100 UG100 μg100 units1100 962 Pieces/Box
Related Pathways




Activin suppresses the expression of inflammatory genes and signaling proteins in human leukemia monocytic THP-1 cells.
ASang Oh Yun, Young Il Kim, Hyung Joon Ahn, Sun Young Min
2801 related Products with: Activin suppresses the expression of inflammatory genes and signaling proteins in human leukemia monocytic THP-1 cells.
100ul1mg1.00 flask1010μg1001010IU10ng 100ul100μg10mg
Related Pathways
-
No related Items




PPARA and IL6: exploring associations with athletic performance and genotype polymorphism.
This study aims to investigate the Interleukin (IL)-6 rs1800795 and peroxisome proliferator-activated receptor alpha (PPARA) rs4253778 polymorphism distributions in the relatively faster and slower subgroups of national cross-country skiing athletes and to identify advantageous genotypes for endurance performance. IL-6 is an inflammatory mediator that is effective in muscle tissue hypertrophy, repair, and the immune system. On the other hand, PPARA transcription factor is a molecule associated with fatty acid, sugar metabolism and inflammation formation. Total of 30 professional cross-country skiing athletes were examined in three groups as athletes, female athletes, and male athletes. DNA of the participants were isolated from blood and genetic polymorphisms were determined by RT-PCR. Athletes were divided into two subgroups as faster and slower referring to their "1-kilometer cross-country skiing time averages (CCSTA)". Polymorphism distributions in these subgroups were analyzed statistically with Fisher's exact test and descriptive tests. In addition, the 1 km-CCSTA values of the genotypes were determined by descriptive statistical methods and the time advantages were calculated. It was determined that the combination of IL-6 rs1800795 GC and PPARA rs4253778 GG genotypes was observed to be more prominent among the faster categories of cross-country skiing competitors, particularly in the athletes and male athletes categories, and it had a time advantage at 1 km-CCSTA. The GC genotype (p= 0.0098) and C-allele (p=0.0398) of IL-6 rs1800795 polymorphism were detected at a higher rate in the fast subgroup in male athletes. These genotypes may support endurance performance.Derya Kazancı, Tolga Polat, Ömer Kaynar, Muhammet Fatih Bilici, Beste Tacal Aslan, Korkut Ulucan
1460 related Products with: PPARA and IL6: exploring associations with athletic performance and genotype polymorphism.
100ug1 g0.1 mg96 wells (1 kit)200ul10 mg100 mg100ug25 mg1000 100 mg 25 MG
Related Pathways




Study on the reversal of epileptic drug resistance by tetramethylpyrazine in combination with carbamazepine through modulation of P-Glycoprotein expression in rat brain microvessel endothelial cell.
The purpose of this study was to detect the changes of P-Glycoprotein (P-GP) expression in rat brain microvessel endothelial cell line RBE4 after the action of Tetramethylpyrazine (TMP) on Carbamazepine (CBZ), so as to clarify the potential mechanism of TMP combined with CBZ against intractable epilepsy drug resistance. The RBE4 cell line was utilized for in vitro analysis. Cells were divided into control, CBZ, and CBZ-TMP group. The expression of P-GP was assessed using Western blot and reverse transcription polymerase chain reaction (RT-PCR). Intracellular concentration of CBZ was measured through high-performance liquid chromatography (HPLC). The differential expression of mRNA was evaluated by RNA sequencing. The intracellular concentration of CBZ in the CBZ-TMP group was significantly higher than that in other groups. The expression of P-GP in the CBZ group was significantly higher than that in the control group, while in the CBZ&TMP group, it was significantly lower than that in the other groups. Comparative analysis also revealed some differentially expressed genes. Compared with the CBZ group, FAM106A, SLC3A2, TENM2, etc. were upregulated most significantly in the CBZ&TMP group. ZBTB10, WDR7, STARD13, etc. were downregulated most significantly. Results suggest that TMP increases the intracellular concentration of CBZ, downregulates the expression of P-GP increased by CBZ, and modulates related cellular metabolism and signaling pathways, thus reversing the drug resistance mechanism of intractable epilepsy, providing a theoretical basis for the combination of traditional Chinese medicine and antiepileptic drugs.Xia Qian, Yuqing Deng, Na Zhong, Yuxuan Li, Junhua Wang, Jinhua Yan, Wei Liu, Jinglei Ye, Jingchao Liu, Guobei Xiao
1304 related Products with: Study on the reversal of epileptic drug resistance by tetramethylpyrazine in combination with carbamazepine through modulation of P-Glycoprotein expression in rat brain microvessel endothelial cell.
96 testscase24 tests100ug Lyophilized1
Related Pathways




Chromatin accessibility and pioneer factor FOXA1 restrict glucocorticoid receptor action in prostate cancer.
Treatment of prostate cancer relies predominantly on the inhibition of androgen receptor (AR) signaling. Despite the initial effectiveness of the antiandrogen therapies, the cancer often develops resistance to the AR blockade. One mechanism of the resistance is glucocorticoid receptor (GR)-mediated replacement of AR function. Nevertheless, the mechanistic ways and means how the GR-mediated antiandrogen resistance occurs have remained elusive. Here, we have discovered several crucial features of GR action in prostate cancer cells through genome-wide techniques. We detected that the replacement of AR by GR in enzalutamide-exposed prostate cancer cells occurs almost exclusively at pre-accessible chromatin sites displaying FOXA1 occupancy. Counterintuitively to the classical pioneer factor model, silencing of FOXA1 potentiated the chromatin binding and transcriptional activity of GR. This was attributed to FOXA1-mediated repression of the NR3C1 (gene encoding GR) expression via the corepressor TLE3. Moreover, the small-molecule inhibition of coactivator p300's enzymatic activity efficiently restricted GR-mediated gene regulation and cell proliferation. Overall, we identified chromatin pre-accessibility and FOXA1-mediated repression as important regulators of GR action in prostate cancer, pointing out new avenues to oppose steroid receptor-mediated antiandrogen resistance.Laura Helminen, Jasmin Huttunen, Melina Tulonen, Niina Aaltonen, Einari A Niskanen, Jorma J Palvimo, Ville Paakinaho
2073 related Products with: Chromatin accessibility and pioneer factor FOXA1 restrict glucocorticoid receptor action in prostate cancer.
Related Pathways




CRISPR-dCas13a system for programmable small RNAs and polycistronic mRNA repression in bacteria.
Bacterial small RNAs (sRNAs) function in post-transcriptional regulatory responses to environmental changes. However, the lack of eukaryotic RNA interference-like machinery in bacteria has limited the systematic engineering of RNA repression. Here, we report the development of clustered regularly interspaced short palindromic repeats (CRISPR)-guided dead CRIPSR-associated protein 13a (dCas13a) ribonucleoprotein that utilizes programmable CRISPR RNAs (crRNAs) to repress trans-acting and cis-acting sRNA as the target, altering regulatory mechanisms and stress-related phenotypes. In addition, we implemented a modular loop engineering of the crRNA to promote modular repression of the target gene with 92% knockdown efficiency and a single base-pair mismatch specificity. With the engineered crRNAs, we achieved targetable single-gene repression in the polycistronic operon. For metabolic application, 102 crRNAs were constructed in the biofoundry and used for screening novel knockdown sRNA targets to improve lycopene (colored antioxidant) production in Escherichia coli. The CRISPR-dCas13a system will assist as a valuable systematic tool for the discovery of novel sRNAs and the fine-tuning of bacterial RNA repression in both scientific and industrial applications.Sung Cheon Ko, Han Min Woo
2337 related Products with: CRISPR-dCas13a system for programmable small RNAs and polycistronic mRNA repression in bacteria.
200ul100 μg 1 G200ul
Related Pathways




ESRP1 controls biogenesis and function of a large abundant multiexon circRNA.
While the majority of circRNAs are formed from infrequent back-splicing of exons from protein coding genes, some can be produced at quite high level and in a regulated manner. We describe the regulation, biogenesis and function of circDOCK1(2-27), a large, abundant circular RNA that is highly regulated during epithelial-mesenchymal transition (EMT) and whose formation depends on the epithelial splicing regulator ESRP1. CircDOCK1(2-27) synthesis in epithelial cells represses cell motility both by diverting transcripts from DOCK1 mRNA production to circRNA formation and by direct inhibition of migration by the circRNA. HITS-CLIP analysis and CRISPR-mediated deletions indicate ESRP1 controls circDOCK1(2-27) biosynthesis by binding a GGU-containing repeat region in intron 1 and detaining its splicing until Pol II completes its 157 kb journey to exon 27. Proximity-dependent biotinylation (BioID) assay suggests ESRP1 may modify the RNP landscape of intron 1 in a way that disfavours communication of exon 1 with exon 2, rather than physically bridging exon 2 to exon 27. The X-ray crystal structure of RNA-bound ESRP1 qRRM2 domain reveals it binds to GGU motifs, with the guanines embedded in clamp-like aromatic pockets in the protein.Dawei Liu, B Kate Dredge, Andrew G Bert, Katherine A Pillman, John Toubia, Wenting Guo, Boris J A Dyakov, Melodie M Migault, Vanessa M Conn, Simon J Conn, Philip A Gregory, Anne-Claude Gingras, Dinshaw Patel, Baixing Wu, Gregory J Goodall
1215 related Products with: ESRP1 controls biogenesis and function of a large abundant multiexon circRNA.
1000 TESTS/0.65ml10 mg200ug200.00 ug10 mg100.00 ug100 mg100ug1,000 tests
Related Pathways




Interrogating two extensively self-targeting Type I CRISPR-Cas systems in Xanthomonas albilineans reveals distinct anti-CRISPR proteins that block DNA degradation.
CRISPR-Cas systems store fragments of invader DNA as spacers to recognize and clear those same invaders in the future. Spacers can also be acquired from the host's genomic DNA, leading to lethal self-targeting. While self-targeting can be circumvented through different mechanisms, natural examples remain poorly explored. Here, we investigate extensive self-targeting by two CRISPR-Cas systems encoding 24 self-targeting spacers in the plant pathogen Xanthomonas albilineans. We show that the native I-C and I-F1 systems are actively expressed and that CRISPR RNAs are properly processed. When expressed in Escherichia coli, each Cascade complex binds its PAM-flanked DNA target to block transcription, while the addition of Cas3 paired with genome targeting induces cell killing. While exploring how X. albilineans survives self-targeting, we predicted putative anti-CRISPR proteins (Acrs) encoded within the bacterium's genome. Screening of identified candidates with cell-free transcription-translation systems and in E. coli revealed two Acrs, which we named AcrIC11 and AcrIF12Xal, that inhibit the activity of Cas3 but not Cascade of the respective system. While AcrF12Xal is homologous to AcrIF12, AcrIC11 shares sequence and structural homology with the anti-restriction protein KlcA. These findings help explain tolerance of self-targeting through two CRISPR-Cas systems and expand the known suite of DNA degradation-inhibiting Acrs.Franziska Wimmer, Frank Englert, Katharina G Wandera, Omer S Alkhnbashi, Scott P Collins, Rolf Backofen, Chase L Beisel
1607 related Products with: Interrogating two extensively self-targeting Type I CRISPR-Cas systems in Xanthomonas albilineans reveals distinct anti-CRISPR proteins that block DNA degradation.
100 μg
Related Pathways




Internal RNA 2'-O-methylation on the HIV-1 genome impairs reverse transcription.
Viral RNA genomes are modified by epitranscriptomic marks, including 2'-O-methylation that is added by cellular or viral methyltransferases. 2'-O-Methylation modulates RNA structure, function and discrimination between self- and non-self-RNA by innate immune sensors such as RIG-I-like receptors. This is illustrated by human immunodeficiency virus type-1 (HIV-1) that decorates its RNA genome through hijacking the cellular FTSJ3 2'-O-methyltransferase, thereby limiting immune sensing and interferon production. However, the impact of such an RNA modification during viral genome replication is poorly understood. Here we show by performing endogenous reverse transcription on methylated or hypomethylated HIV-1 particles, that 2'-O-methylation negatively affects HIV-1 reverse transcriptase activity. Biochemical assays confirm that RNA 2'-O-methylation impedes reverse transcriptase activity, especially at low dNTP concentrations reflecting those in quiescent cells, by reducing nucleotide incorporation efficiency and impairing translocation. Mutagenesis highlights K70 as a critical amino acid for the reverse transcriptase to bypass 2'-O-methylation. Hence, the observed antiviral effect due to viral RNA 2'-O-methylation antagonizes the FTSJ3-mediated proviral effects, suggesting the fine-tuning of RNA methylation during viral replication.Alice Decombe, Olve Peersen, Priscila Sutto-Ortiz, Célia Chamontin, Géraldine Piorkowski, Bruno Canard, Sébastien Nisole, Etienne Decroly
2588 related Products with: Internal RNA 2'-O-methylation on the HIV-1 genome impairs reverse transcription.
100ug100 μg1000 units5 X 1000 U 100ul1000 units 100ul 25 MG1000 units
Related Pathways




Hi-BDiSCO: folding 3D mesoscale genome structures from Hi-C data using brownian dynamics.
The structure and dynamics of the eukaryotic genome are intimately linked to gene regulation and transcriptional activity. Many chromosome conformation capture experiments like Hi-C have been developed to detect genome-wide contact frequencies and quantify loop/compartment structures for different cellular contexts and time-dependent processes. However, a full understanding of these events requires explicit descriptions of representative chromatin and chromosome configurations. With the exponentially growing amount of data from Hi-C experiments, many methods for deriving 3D structures from contact frequency data have been developed. Yet, most reconstruction methods use polymer models with low resolution to predict overall genome structure. Here we present a Brownian Dynamics (BD) approach termed Hi-BDiSCO for producing 3D genome structures from Hi-C and Micro-C data using our mesoscale-resolution chromatin model based on the Discrete Surface Charge Optimization (DiSCO) model. Our approach integrates reconstruction with chromatin simulations at nucleosome resolution with appropriate biophysical parameters. Following a description of our protocol, we present applications to the NXN, HOXC, HOXA and Fbn2 mouse genes ranging in size from 50 to 100 kb. Such nucleosome-resolution genome structures pave the way for pursuing many biomedical applications related to the epigenomic regulation of chromatin and control of human disease.Zilong Li, Tamar Schlick
1270 related Products with: Hi-BDiSCO: folding 3D mesoscale genome structures from Hi-C data using brownian dynamics.
Related Pathways
Contact Us:
Belgium
Voortstraat 49, 1910 Kampenhout BELGIUM
Tel 0032 16 58 90 45 Fax 0032 16 50 90 45
[email protected]
France
9, rue Lagrange, 75005 Paris
Tel 01 43 25 01 50 Fax 01 43 25 01 60
[email protected]
Germany
GENTAUR GmbH
Marienbongard 20
52062 Aachen Deutschland
Tel 0241 40 08 90 86 Fax 0241 55 91 05 36
[email protected]
United Kingdom
GENTAUR Ltd.
Howard Frank Turnberry House
1404-1410 High Road
Whetstone London N20 9BH
Tel 020 3393 8531 Fax 020 8445 9411
[email protected]
Also in
Luxembourg +35220880274
Schweiz Züri +41435006251
Danmark +4569918806
Österreich +43720880899
Česká republika Praha +420246019719
Ireland Dublin +35316526556
Norge Oslo +4721031366
Finland Helsset +358942419041
Sverige Stockholm +46852503438
Ελλάς Αθήνα +302111768494
Magyarország Budapest +3619980547
Poland
GENTAUR Poland Sp. z o.o.
ul. Grunwaldzka 88/A m.2
81-771 Sopot, Poland
Tel 058 710 33 44
Fax 058 710 33 48
[email protected]
skype gentaurpoland
Nederland
GENTAUR Nederland BV
Kuiper 1
5521 DG Eersel Nederland
Tel 0208-080893 Fax 0497-517897
[email protected]
Italy
GENTAUR SRL
IVA IT03841300167
Piazza Giacomo Matteotti, 6, 24122 Bergamo
Tel 02 36 00 65 93 Fax 02 36 00 65 94
[email protected]
Spain
GENTAUR Spain
Tel 0911876558
[email protected]
Bulgaria
GENTAUR Bulgaria
53 Iskar Str. 1191 Kokalyane, Sofia
Sofia 1000
Tel 0035924682280
Fax 0035929830072
[email protected]