Only in Titles

           Search results for: 3-Azidobenzoic Acid C7H5N3O2 CAS: 1843-35-2   

paperclip

#29341880   // Save this To Up

Targetable long non-coding RNAs in cancer treatments.

Aberrant expression of many long non-coding RNAs has been observed in various types of cancer, implicating their crucial roles in tumorigenesis and cancer progression. Emerging knowledge with regard to the critical physiological and pathological roles of long non-coding RNAs in cancers makes them potential targets in cancer treatments. In this review, we present a summary of the relatively well studied long non-coding RNAs that are involved in oncogenesis and outline their functions and functional mechanisms. Recent findings that may be utilized in therapeutic intervention are also highlighted. With the fast development in nucleic acid-based therapeutic reagents that can target disease associated RNAs, lncRNAs should be explored as potential targets in cancer treatments.

1883 related Products with: Targetable long non-coding RNAs in cancer treatments.

Cancer Apoptosis Phospho- Top five cancer tissue ar Multiple organ cancer tis Lung cancer tissue array, Lung cancer tissue array Colon cancer and normal t Colon cancer and normal t Colon cancer, metastasize Colon cancer and matched Colon cancer tissue array Rectum disease spectrum ( Kidney disease spectrum (

Related Pathways

paperclip

#29337866   // Save this To Up

CRISPR-Cas Targeting of Host Genes as an Antiviral Strategy.

Currently, a new gene editing tool-the Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR) associated (Cas) system-is becoming a promising approach for genetic manipulation at the genomic level. This simple method, originating from the adaptive immune defense system in prokaryotes, has been developed and applied to antiviral research in humans. Based on the characteristics of virus-host interactions and the basic rules of nucleic acid cleavage or gene activation of the CRISPR-Cas system, it can be used to target both the virus genome and host factors to clear viral reservoirs and prohibit virus infection or replication. Here, we summarize recent progress of the CRISPR-Cas technology in editing host genes as an antiviral strategy.

1599 related Products with: CRISPR-Cas Targeting of Host Genes as an Antiviral Strategy.

Astrovirus antibody, Mono ASK1 (Phospho Ser83) Anti ASK1 (Phospho Ser966) Ant ASK1 (Ab 83) Antibody Hos ASK1 (Ab 966) Antibody Ho Caspase 3 antibody Host S Caspase 8 antibody Host S Caspase 9 antibody Host S Cultrex In Vitro Angiogen Mouse AntiTAP (tip associ Mouse AntiHEF1 CasL Targe Mouse AntiHEF1 CasL Targe

Related Pathways

paperclip

#29335517   // Save this To Up

A versatile MOF-based trap for heavy metal ion capture and dispersion.

Current technologies for removing heavy metal ions are typically metal ion specific. Herein we report the development of a broad-spectrum heavy metal ion trap by incorporation of ethylenediaminetetraacetic acid into a robust metal-organic framework. The capture experiments for a total of 22 heavy metal ions, covering hard, soft, and borderline Lewis metal ions, show that the trap is very effective, with removal efficiencies of >99% for single-component adsorption, multi-component adsorption, or in breakthrough processes. The material can also serve as a host for metal ion loading with arbitrary selections of metal ion amounts/types with a controllable uptake ratio to prepare well-dispersed single or multiple metal catalysts. This is supported by the excellent performance of the prepared Pd2+-loaded composite toward the Suzuki coupling reaction. This work proposes a versatile heavy metal ion trap that may find applications in the fields of separation and catalysis.

1815 related Products with: A versatile MOF-based trap for heavy metal ion capture and dispersion.

Rabbit Anti-Metal ion tra Rabbit Anti-Metal ion tra Rabbit Anti-Metal ion tra Rabbit Anti-Metal ion tra Rabbit Anti-Metal ion tra Rabbit Anti-Metal ion tra Rabbit Anti-Metal ion tra Rabbit Anti-Metal ion tra Rabbit Anti-Metal ion tra Rabbit Anti-Metal ion tra Rabbit Anti-Metal ion tra Rabbit Anti-Metal ion tra

Related Pathways

paperclip

#29334087   // Save this To Up

Achiral non-fluorescent molecule assisted enhancement of circularly polarized luminescence in naphthalene substituted histidine organogels.

A naphthalene substituted histidine derivative was found to form an organogel showing circularly polarized luminescence (CPL) and the addition of non-fluorescent achiral benzoic acids could efficiently enhance the CPL via non-covalent interactions.

1615 related Products with: Achiral non-fluorescent molecule assisted enhancement of circularly polarized luminescence in naphthalene substituted histidine organogels.

Human intercellular adhes Mouse intercellular adhes Human Kidney injury molec 5 (2 Aminoethylamino) 1 n 5 (2 Aminoethylamino) 1 n 3 Phenylumbelliferone, Fl 6 para Toluidino 2 naphth 6 para Toluidino 2 naphth 11 (4,4 difluoro 5,7 dime Influenza A H5N1 (Avian) Influenza A H5N1 (Avian) Influenza A H5N1 (Avian)

Related Pathways

paperclip

#29332828   // Save this To Up

UPLC-MS/MS analysis for antioxidant components of Lycii Fructus based on spectrum-effect relationship.

Lycii Fructus is widely cultivated in the Northwest China. It is well-known for its antiaging effect in traditional Chinese medicines (TCMs), but the effective components are not clear. In this work, the ultra-performance liquid chromatography tandem mass spectrometry (UPLC-MS/MS) was used to study the antioxidant components of Lycii Fructus through analyzing the spectrum-effect relationship, and the positive correlation components with antioxidant activity were partially identified. The extractums of Lycii Fructus were adsorbed with macroporous resin, and then eluted with water and 30%, 60%, 90% ethanol in turn. The extract fraction eluted with 60% ethanol was determined as the best, and was taken for subsequent experiments. With the above separation method, UPLC fingerprints of thirty batches of Lycii Fructus (from different areas) were obtained, and thirty common peaks were selected through similarity analysis (SA). Combined with the data of the 2,2-diphenyl-1-picrylhydrazyl (DPPH) and 2,2'-azino-bis (3-ethylbenzothiazoline-6-sulfonic acid) diammonium salt (ABTS) assays, the spectrum-effect relationship was studied. The results showed that the main peaks with antioxidant activity were P14, P26, P8, and P21 for DPPH, and P26, P14, P21, and P19 for ABTS. Using the UPLC-MS/MS data, peaks P14, P19, P21, and P30 were respectively identified as chlorogenic acid, quercetin, kaempferol, and isorhamnetin, and then the results were confirmed through comparison with the standards and other references. Finally, their strong antioxidant activities were validated experimentally.

2492 related Products with: UPLC-MS/MS analysis for antioxidant components of Lycii Fructus based on spectrum-effect relationship.

MarkerGeneTM Fluorescent Cellufine Formyl , 50 ml Cellufine Formyl Media Cellufine Formyl , 500 ml Cellufine Formyl Media Cellufine Formyl Media Bcl-2 Oncoprotein; Clone Bcl-2 Oncoprotein; Clone c-erbB-2 Oncoprotein c-erbB-2 Oncoprotein c-erbB-3 Oncoprotein; Cl c-erbB-3 Oncoprotein; Cl

Related Pathways

  •  
  • No related Items
paperclip

#29331071   // Save this To Up

Hepatic PPARα function is controlled by polyubiquitination and proteasome-mediated degradation via the coordinated actions of PAQR3 and HUWE1.

Peroxisome proliferator-activated receptor α (PPARα) is a key transcriptional factor that regulates hepatic lipid catabolism by stimulating fatty acid oxidation and ketogenesis in an adaptive response to nutrient starvation. However, how PPARα is regulated by post-translational modification is poorly understood. Here, we identified that PAQR3 promotes PPARα ubiquitination through the E3 ubiquitin ligase HUWE1, thereby negatively modulating PPARα functions both in vitro and in vivo. Adenovirus-mediated Paqr3 knockdown and liver-specific deletion of the Paqr3 gene reduced hepatic triglyceride levels while increasing fatty acid oxidation and ketogenesis upon fasting. PAQR3 deficiency enhances the fasting-induced expression of PPARα target genes, including those involved in fatty acid oxidation and FGF21, a key molecule that mediates the metabolism-modulating effects of PPARα. PAQR3 directly interacts with PPARα and increases the polyubiquitination and proteasome-mediated degradation of PPARα. Furthermore, the E3 ubiquitin ligase HUWE1 was identified to mediate PPARα polyubiquitination. Additionally, PAQR3 enhances the interaction between HUWE1 and PPARα. Collectively, this study revealed that ubiquitination modification through the coordinated action of PAQR3 with HUWE1 plays a crucial role in regulating the activity of PPARα in response to starvation. This article is protected by copyright. All rights reserved.

2693 related Products with: Hepatic PPARα function is controlled by polyubiquitination and proteasome-mediated degradation via the coordinated actions of PAQR3 and HUWE1.

Androgen Receptor (Phosph Androgen Receptor (Phosph Rabbit Anti-Human Androge Rabbit Anti-Human Androge Androgen Receptor (Ab 650 AZD-3514 Mechanisms: Andr 17β-Acetoxy-2α-bromo-5 (5α,16β)-N-Acetyl-16-[2 (5α,16β)-N-Acetyl-16-ac 5α-N-Acetyl-2'H-androst- 5α-N-Acetyl-2'H-androst- 3-O-Acetyl 5,14-Androstad

Related Pathways

paperclip

#29330181   // Save this To Up

A Novel l-Glutamate Exporter of Corynebacterium glutamicum.

Besides metabolic pathways and regulatory networks, transport systems are also pivotal for cellular metabolism and hyper-production of biochemicals using microbial cell factories. Identification and characterization of transporters are therefore of great significance for understanding and engineering of transport reactions. Herein, a novel l-glutamate exporter MscCG2 that extensively exists in Corynebacterium glutamicum strains but is distinct from the only known l-glutamate exporter MscCG was discovered in an industrial l-glutamate producing C. glutamicum MscCG2 was predicted to possess three transmembrane helices in the N-terminal region and located in the cytoplasmic membrane, which are typical structural characteristics of the mechanosensitive channel of small conductance. MscCG2 has a low amino acid sequence identity (23%) to MscCG and evolved separately from MscCG with four transmembrane helices. Despite the considerable differences between MscCG2 and MscCG in sequence and structure, gene deletion and complementation confirmed that MscCG2 also functioned as an l-glutamate exporter and an osmotic safety valve in C. glutamicum Besides, transcriptional analysis showed that MscCG2 and MscCG genes were transcribed in similar patterns and not induced by l-glutamate producing conditions. It was also demonstrated that MscCG2-mediated l-glutamate excretion was activated by biotin limitation or penicillin treatment and constitutive l-glutamate excretion was triggered by gain-of-function mutation of MscCG2 (A151V). Discovery of MscCG2 will enrich the understanding of bacterial amino acid transport and provide additional targets for exporter engineering.IMPORTANCEExchange of matter, energy and information with surroundings is fundamental for cellular metabolism. Therefore, studying transport systems that are essential for these processes is of great significance. Besides, transport systems of bacterial cells are usually related to product excretion as well as product re-uptake, making transporter engineering a useful strategy for strain improvement. The significance of our research is in identifying and characterizing a novel l-glutamate exporter from the industrial workhorse Corynebacterium glutamicum, which will enrich the understanding of l-glutamate excretion and provide a new target for studying bacterial amino acid transport and engineering transport reactions.

1258 related Products with: A Novel l-Glutamate Exporter of Corynebacterium glutamicum.

Anti VGLUT 1 Rat, polyclo Anti Rat VGLUT 2, Rabbit Glutamate receptor 2 (Pre Amplite™ Fluorimetric G Rabbit Anti-Rat Metabotro Glutamate receptor 2 (Pre Rabbit anti Glutamate rec QuantiChrom™ Glutamate EnzyChrom™ Glutamate As Glutamate Assay Kit Glutamate Dehydrogenase A Rabbit anti Glutamate rec

Related Pathways

paperclip

#29329795   // Save this To Up

Omega-3 fatty acids and adipose tissue biology.

This review provides evidence for the importance of white and brown adipose tissue (i.e. WAT and BAT) function for the maintenance of healthy metabolic phenotype and its preservation in response to omega-3 polyunsaturated fatty acids (omega-3 PUFA), namely in the context of diseased states linked to aberrant accumulation of body fat, systemic low-grade inflammation, dyslipidemia and insulin resistance. More specifically, the review deals with (i) the concept of immunometabolism, i.e. how adipose-resident immune cells and adipocytes affect each other and define the immune-metabolic interface; and (ii) the characteristic features of "healthy adipocytes" in WAT, which are relatively small fat cells endowed with a high capacity for mitochondrial oxidative phosphorylation, triacylglycerol/fatty acid (TAG/FA) cycling and de novo lipogenesis (DNL). The intrinsic metabolic features of WAT and their flexible regulations, reflecting the presence of "healthy adipocytes", provide beneficial local and systemic effects, including (i) protection against in situ endoplasmic reticulum stress and related inflammatory response during activation of adipocyte lipolysis; (ii) prevention of ectopic fat accumulation and dyslipidemia caused by increased hepatic VLDL synthesis, as well as prevention of lipotoxic damage of insulin signaling in extra-adipose tissues; and also (iii) increased synthesis of anti-inflammatory and insulin-sensitizing lipid mediators with pro-resolving properties, including the branched fatty acid esters of hydroxy fatty acids (FAHFAs), also depending on the activity of DNL in WAT. The "healthy adipocytes" phenotype can be induced in WAT of obese mice in response to various stimuli including dietary omega-3 PUFA, especially when combined with moderate calorie restriction, and possibly also with other life style (e.g. physical activity) or pharmacological (e.g. thiazolidinediones) interventions. While omega-3 PUFA could exert beneficial systemic effects by improving immunometabolism of WAT without a concomitant induction of BAT, it is currently not clear whether the metabolic effects of the combined intervention using omega-3 PUFA and calorie restriction or thiazolidinediones depend also on the activation of BAT function and/or the induction of brite/beige adipocytes in WAT. It remains to be established why omega-3 PUFA intervention in type 2 diabetic subjects does not improve insulin sensitivity and glucose homeostasis despite inducing various anti-inflammatory mediators in WAT, including the recently discovered docosahexaenoic esters of hydroxy linoleic acid, the lipokines from the FAHFAs family, as well as several endocannabinoid-related anti-inflammatory lipids. To answer the question whether and to which extent omega-3 PUFA supplementation could promote the formation of "healthy adipocytes" in WAT of human subjects, namely in the obese insulin-resistant patients, represents a challenging task that is of great importance for the treatment of some serious non-communicable diseases.

2155 related Products with: Omega-3 fatty acids and adipose tissue biology.

Triglyceride Assay Kit Li AZD-3514 Mechanisms: Andr 17β-Acetoxy-2α-bromo-5 3-O-Acetyl 5,14-Androstad 3-O-Acetyl-17-O-tert-buty 3β-O-Acetyl-androsta-5,1 5α-Androstan-3β-ol � ∆1-Androstene-3α,17β- ∆1-Androstene-3α,17β- ∆1-Androstene-3β,17β- Androsta-1,4,6-triene-3,1 (3β)-Androsta-5,16-diene

Related Pathways

paperclip

#29327679   // Save this To Up

Natural and Artificial Strategies To Control the Conjugative Transmission of Plasmids.

Conjugative plasmids are the main carriers of transmissible antibiotic resistance (AbR) genes. For that reason, strategies to control plasmid transmission have been proposed as potential solutions to prevent AbR dissemination. Natural mechanisms that bacteria employ as defense barriers against invading genomes, such as restriction-modification or CRISPR-Cas systems, could be exploited to control conjugation. Besides, conjugative plasmids themselves display mechanisms to minimize their associated burden or to compete with related or unrelated plasmids. Thus, FinOP systems, composed of FinO repressor protein and FinP antisense RNA, aid plasmids to regulate their own transfer; exclusion systems avoid conjugative transfer of related plasmids to the same recipient bacteria; and fertility inhibition systems block transmission of unrelated plasmids from the same donor cell. Artificial strategies have also been designed to control bacterial conjugation. For instance, intrabodies against R388 relaxase expressed in recipient cells inhibit plasmid R388 conjugative transfer; pIII protein of bacteriophage M13 inhibits plasmid F transmission by obstructing conjugative pili; and unsaturated fatty acids prevent transfer of clinically relevant plasmids in different hosts, promoting plasmid extinction in bacterial populations. Overall, a number of exogenous and endogenous factors have an effect on the sophisticated process of bacterial conjugation. This review puts them together in an effort to offer a wide picture and inform research to control plasmid transmission, focusing on Gram-negative bacteria.

2008 related Products with: Natural and Artificial Strategies To Control the Conjugative Transmission of Plasmids.

FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu NATtrol TOXOPLASMA GONDII Head & Neck cancer test t High density tissue array EZH2 KMT6 Control Peptid GFP control peptide anti GFP Control Peptide Topoisomerase II; Clone Topoisomerase II; Clone

Related Pathways

paperclip

#29325806   // Save this To Up

RIFM fragrance ingredient safety assessment, pentanedioic acid, 1,5-dimethyl ester, CAS Registry Number 1119-40-0.


1971 related Products with: RIFM fragrance ingredient safety assessment, pentanedioic acid, 1,5-dimethyl ester, CAS Registry Number 1119-40-0.

(4S,6R)-6-(Acetoxymethyl) 5-O-Acetyl-4-O-benzyloyl- (11α,13E,17S)-9-O-Acetyl (2S,4S)-4-(Acetylthio)-2- N-[3-Amino-1-(cyclobutylm N-(2-Aminoethyl)-N-methyl (4R-cis)-6-Aminomethyl-2, (2S,4S)-4-Amino-1,2-pyrro N-(1α,5α,6α)-3-Αzabic (2S,4R)-4-Azido-1,2-pyrro (1S,3R)-1-Benzo[1,3]dioxo Benz[a]anthracene-7-aceti

Related Pathways

  •  
  • No related Items