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           Search results for: miRNASelect™ pEGP_mmu_mir_382 Expression Vector   

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Inhibition of hepatitis B virus replication via HBV DNA cleavage by Cas9 from Staphylococcus aureus.

Chronic hepatitis B virus (HBV) infection is difficult to cure due to the presence of covalently closed circular DNA (cccDNA). Accumulating evidence indicates that the CRISPR/Cas9 system effectively disrupts HBV genome, including cccDNA, in vitro and in vivo. However, efficient delivery of CRISPR/Cas9 system to the liver or hepatocytes using an adeno-associated virus (AAV) vector remains challenging due to the large size of Cas9 from Streptococcus pyogenes (Sp). The recently identified Cas9 protein from Staphylococcus aureus (Sa) is smaller than SpCas9 and thus is able to be packaged into the AAV vector. To examine the efficacy of SaCas9 system on HBV genome destruction, we designed 5 guide RNAs (gRNAs) that targeted different HBV genotypes, 3 of which were shown to be effective. The SaCas9 system significantly reduced HBV antigen expression, as well as pgRNA and cccDNA levels, in Huh7, HepG2.2.15 and HepAD38 cells. The dual expression of gRNAs/SaCas9 in these cell lines resulted in more efficient HBV genome cleavage. In the mouse model, hydrodynamic injection of gRNA/SaCas9 plasmids resulted in significantly lower levels of HBV protein expression. We also delivered the SaCas9 system into mice with persistent HBV replication using an AAV vector. Both the AAV vector and the mRNA of Cas9 could be detected in the C3H mouse liver cells. Decreased hepatitis B surface antigen (HBsAg), HBV DNA and pgRNA levels were observed when a higher titer of AAV was injected, although this decrease was not significantly different from the control. In summary, the SaCas9 system accurately and efficiently targeted the HBV genome and inhibited HBV replication both in vitro and in vivo. The system was delivered by an AAV vector and maybe used as a novel therapeutic strategy against chronic HBV infection.

2680 related Products with: Inhibition of hepatitis B virus replication via HBV DNA cleavage by Cas9 from Staphylococcus aureus.

Viral antibodies, anti-R anti Rotavirus p42 IgG2a Rabbit Anti-Polyprotein(H Rabbit Anti-Hepatitis C V Rabbit Anti-Hepatitis C V Staphylococcus Aureus Rea ACTGene Blue Hot Start DN HbcAg - Hepatitis B Viru HbcAg - Hepatitis B Viru HbcAg - Hepatitis B Viru Protease, DNASE free hea Protease, DNASE free hea

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Silencing of Iron and Heme-Related Genes Revealed a Paramount Role of Iron in the Physiology of the Hematophagous Vector.

Iron is an essential element for most organisms However, free iron and heme, its complex with protoporphyrin IX, can be extremely cytotoxic, due to the production of reactive oxygen species, eventually leading to oxidative stress. Thus, eukaryotic cells control iron availability by regulating its transport, storage and excretion as well as the biosynthesis and degradation of heme. In the genome of, the vector of Chagas disease, we identified 36 genes related to iron and heme metabolism We performed a comprehensive analysis of these genes, including identification of homologous genes described in other insect genomes. We observed that blood-meal modulates the expression of ferritin, Iron Responsive protein (IRP), Heme Oxygenase (HO) and the heme exporter Feline Leukemia Virus C Receptor (FLVCR), components of major pathways involved in the regulation of iron and heme metabolism, particularly in the posterior midgut (PM), where an intense release of free heme occurs during the course of digestion. Knockdown of these genes impacted the survival of nymphs and adults, as well as molting, oogenesis and embryogenesis at different rates and time-courses. The silencing of FLVCR caused the highest levels of mortality in nymphs and adults and reduced nymph molting. The oogenesis was mildly affected by the diminished expression of all of the genes whereas embryogenesis was dramatically impaired by the knockdown of ferritin expression. Furthermore, an intense production of ROS in the midgut of blood-fed insects occurs when the expression of ferritin, but not HO, was inhibited. In this manner, the degradation of dietary heme inside the enterocytes may represent an oxidative challenge that is counteracted by ferritins, conferring to this protein a major antioxidant role. Taken together these results demonstrate that the regulation of iron and heme metabolism is of paramount importance forphysiology and imbalances in the levels of these key proteins after a blood- meal can be extremely deleterious to the insects in their various stages of development.

1407 related Products with: Silencing of Iron and Heme-Related Genes Revealed a Paramount Role of Iron in the Physiology of the Hematophagous Vector.

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The E3 ubiquitin ligase NEDD4 mediates cell migration signaling of EGFR in lung cancer cells.

EGFR-dependent cell migration plays an important role in lung cancer progression. Our previous study observed that the HECT E3 ubiquitin ligase NEDD4 is significantly correlated with tumor metastasis and required for migration and invasion signaling of EGFR in gastric cancer cells. However, how NEDD4 promotes the EGFR-dependent lung cancer cell migration is unknown. This study is to elucidate the mechanism by which NEDD4 mediates the EGFR lung cancer migration signaling.

2233 related Products with: The E3 ubiquitin ligase NEDD4 mediates cell migration signaling of EGFR in lung cancer cells.

Lung non small cell cance Non-small cell lung cance anti HSV (II) gB IgG1 (mo anti HCMV IE pp65 IgG1 (m anti HCMV gB IgG1 (monocl Macrophage Colony Stimula Macrophage Colony Stimula GLP 1 ELISA Kit, Rat Gluc GLP 2 ELISA Kit, Rat Prog Glucagon ELISA KIT, Rat G Leptin ELISA Kit, Rat Lep CometAssay Electrophoresi

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Heterologous expression of rTsHyal-1: the first recombinant hyaluronidase of scorpion venom produced in Pichia pastoris system.

In general, hyaluronidases have a broad potential application on medicine and esthetics fields. Hyaluronidases from animal venoms cleave hyaluronan present in the extracellular matrix, acting as spreading factors of toxins into the tissues of the victim. However, the in-depth characterization of hyaluronidase from animal venoms has been neglected due to its instability and low concentration in the venom, which hamper its isolation. Thus, heterologous expression of hyaluronidase acts as a biotechnological tool in the obtainment of enough amounts of the enzyme for structural and functional studies. Therefore, this study produced a recombinant hyaluronidase from Tityus serrulatus scorpion venom, designated as rTsHyal-1, in the Pichia pastoris system. Thus, a gene for TsHyal-1 (gb|KF623285.1) was synthesized and cloned into the pPICZαA vector (GenScript Corporation) for heterologous expression in P. pastoris. rTsHyal-1 was expressed in laboratorial scale in a buffered minimal medium containing methanol (BMM) for 96 h with daily addition of methanol. Expression of rTsHyal-1 resulted in a total protein yield of 0.266 mg/mL. rTsHyal-1 partially purified through cation exchange chromatography presented a specific activity of 1097 TRU/mg, against 838 TRU/mg for the final expressed material, representing a 1.31-fold purification. rTsHyal-1 has molecular mass of 49.5 kDa, and treatment with PNGase F and analysis by mass spectrometry (MALDI-TOF) indicated a potential N-glycosylation of 4.5 kDa. Additionally, de novo sequencing of rTsHyal-1, performed in MALDI-TOF and Q Exactive Orbitrap MS, resulted in 46.8% of protein sequence coverage. rTsHyal-1 presents the highest substrate specificity to hyaluronan followed by chondroitin-6-sulfate, chondroitin-4-sulfate, and dermatan sulfate and showed an optimum activity at pH 6.0 and 40 °C. These results validate the biotechnological process for the heterologous expression of rTsHyal-1. This is the first recombinant hyaluronidase from scorpion venoms expressed in the P. pastoris system with preserved enzyme activity.

1179 related Products with: Heterologous expression of rTsHyal-1: the first recombinant hyaluronidase of scorpion venom produced in Pichia pastoris system.

HBV surface recombinant a HBV surface recombinant a Recombinant Mn SOD (Human Allergens, Phospholipase anti GSK3 Beta IgG2a (mon anti HIV 2 gp36 IgG1 (mon anti HIV 1 p24 IgG1 (mono anti HIV 1 p55 17 IgG1 (m anti HIV 1 p17 IgG1 (mono anti HIV 1 gp41 IgG1 (mon anti HCV core IgG2a (mono anti HCV core IgG2a (mono

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Oral engineered Bifidobacterium longum expressing rhMnSOD to suppress experimental colitis.

In recent years, using genetic engineering and bioengineering techniques, Bifidobacterium as a carrier to express specific functions of the protein or polypeptide, has become a new treatment for disease. Ulcerative colitis (UC) is a type of inflammatory bowel diseases (IBD). Although the cause of this inflammatory disorder is still unknown, a large amount of evidence suggests that ulcerative colitis is associated with increased activity of reactive oxygen species (ROS), manganese superoxide dismutase (MnSOD) is a kind of superoxide dismutase (SOD) has been demonstrated to play a key role in the pathophysiology of colitis. Here, we explored the Bifidobacterium as a drug delivery system to orally deliver a potent anti-inflammatory but poor penetration and stability antioxidant enzymes human MnSOD, transported into cells by a penetratin PEP-1. We constructed an expression vector expressing PEP-1-hMnSOD fusion protein, and successfully expressed hMnSOD fusion protein in engineered Bifidobacterium. Then we identified the bioactivity of engineered Bifidobacterium in LPS-induced inflammatory cell model. Finally, we used Bifidobacterium expressing PEP-1-hMnSOD fusion protein against DSS-induced ulcerative colitis mice. B. longum-PEP-1-rhMnSOD can successfully express rhMnSOD in the colon. We found that levels of inflammatory cytokines TNF-α, IL-1β, IL-6 and IL-8 as well as histological damage in colonic tissues showed that engineered Bifidobacterium effectively reduced dextran sulfate sodium(DSS)-induced ulcerative colitis, we also tested the MPO, verified the above conclusions. These results suggest that oral Bifidobacterium expressing PEP-1-hMnSOD fusion protein can be treated as a new method of UC treatment.

1415 related Products with: Oral engineered Bifidobacterium longum expressing rhMnSOD to suppress experimental colitis.

Oral cavity (tongue and p Oral squamous cell cancer Topoisomerase II; Clone Topoisomerase II; Clone Topoisomerase II; Clone Toludine Blue Solution Toludine Blue Solution Toludine Blue Solution Toxoplasma gondii MIC 3 r Toxoplasma gondii P24 (GR Toxoplasma gondii P29 (GR Toxoplasma gondii P30 (SA

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Oxidative damage and response to Bacillus Calmette-Guérin in bladder cancer cells expressing sialyltransferase ST3GAL1.

Treatment with Bacillus Calmette-Guérin (BCG) is the gold standard adjuvant immunotherapy of non-muscle invasive bladder cancer (NMIBC), although it fails in one third of the patients. NMIBC expresses two tumor-associated O-linked carbohydrates: the disaccharide (Galβ1,3GalNAc) Thomsen-Friedenreich (T) antigen, and its sialylated counterpart (Siaα2,3Galβ1,3GalNAc) sialyl-T (sT), synthesized by sialyltransferase ST3GAL1, whose roles in BCG response are unknown.

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Top five cancer tissue ar Bladder cancer tissue arr Bladder cancer tissue arr Bladder cancer and normal Bladder cancer tissue arr Mid advanced stage bladde Bladder cancer tissue arr Bladder cancer tissue arr Bladder cancer tissue arr Mid advanced stage bladde Bladder cancer tissue arr GFP Expressing Human Inte

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Cell-type specific expression of constitutively-active Rheb promotes regeneration of bulbospinal respiratory axons following cervical SCI.

Damage to respiratory neural circuitry and consequent loss of diaphragm function is a major cause of morbidity and mortality in individuals suffering from traumatic cervical spinal cord injury (SCI). Repair of CNS axons after SCI remains a therapeutic challenge, despite current efforts. SCI disrupts inspiratory signals originating in the rostral ventral respiratory group (rVRG) of the medulla from their phrenic motor neuron (PhMN) targets, resulting in loss of diaphragm function. Using a rat model of cervical hemisection SCI, we aimed to restore rVRG-PhMN-diaphragm circuitry by stimulating regeneration of injured rVRG axons via targeted induction of Rheb (ras homolog enriched in brain), a signaling molecule that regulates neuronal-intrinsic axon growth potential. Following C2 hemisection, we performed intra-rVRG injection of an adeno-associated virus serotype-2 (AAV2) vector that drives expression of a constitutively-active form of Rheb (cRheb). rVRG neuron-specific cRheb expression robustly increased mTOR pathway activity within the transduced rVRG neuron population ipsilateral to the hemisection, as assessed by levels of phosphorylated ribosomal S6 kinase. By co-injecting our novel AAV2-mCherry/WGA anterograde/trans-synaptic axonal tracer into rVRG, we found that cRheb expression promoted regeneration of injured rVRG axons into the lesion site, while we observed no rVRG axon regrowth with AAV2-GFP control. AAV2-cRheb also significantly reduced rVRG axonal dieback within the intact spinal cord rostral to the lesion. However, cRheb expression did not promote any recovery of ipsilateral hemi-diaphragm function, as assessed by inspiratory electromyography (EMG) burst amplitudes. This lack of functional recovery was likely because regrowing rVRG fibers did not extend back into the caudal spinal cord to synaptically reinnervate PhMNs that we retrogradely-labeled with cholera toxin B from the ipsilateral hemi-diaphragm. Our findings demonstrate that enhancing neuronal-intrinsic axon growth capacity can promote regeneration of injured bulbospinal respiratory axons after SCI, but this strategy may need to be combined with other manipulations to achieve reconnection of damaged neural circuitry and ultimately recovery of diaphragm function.

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MOUSE ANTI BOVINE ROTAVIR DNA (cytosine 5) methyltr T-cell proliferation grad TCCI T cell proliferation TCCI T cell proliferation T-cell proliferation grad TCBI T cell proliferation TCBI T cell proliferation T-cell proliferation grad TCPI T cell proliferation TCPI T cell proliferation T-cell proliferation grad

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The rice "fruit-weight 2.2-like" gene family member OsFWL4 is involved in the translocation of cadmium from roots to shoots.

Heterogeneous expression of the rice genes "fruit-weight 2.2-like" (OsFWL) affects Cd resistance in yeast, and OsFWL4 mediates the translocation of Cd from roots to shoots. Cadmium (Cd) induces chronic and toxic effects in humans. In a previous study (Xu et al. in Planta 238:643-655, 2013), we cloned the rice genes, designated OsFWL1-8, homologous to the tomato fruit-weight 2.2. Here, we show that expression of genes OsFWL3-7 in yeast confers resistance to Cd. The Cd contents of OsFWL3-, -4-, -6- and -7-transformed Cd(II)-sensitive yeast mutant ycf1 cells were strongly decreased compared with those of empty vector, with the strongest resistance to Cd observed in cells expressing OsFWL4. Evaluation of truncated and site-directed mutation derivatives revealed that the CCXXG motifs near the second transmembrane region of OsFWL4 are involved in Cd resistance in yeast. Real-time PCR analysis showed that OsFWL4 expression was induced by CdClstress in rice seedlings. Compared with WT plants, the Cd contents in the shoots of RNAi mediated OsFWL4 knockdown plants were significantly decreased, and Cd translocation from roots to shoots was reduced. According to bimolecular fluorescence complementation, yeast two-hybrid and Western-blotting assays, the OsFWL4 protein forms homo-oligomers. These results suggest that OsFWL4 might act directly as a transporter and is involved in the translocation of Cd from roots to shoots in rice.

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Interleukin-34 IL34 (N-t Interleukin-34 IL34 anti FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu amyloid beta precursor pr (R,R)-N-(2-Amino-1,2-diph (3S,4aS,8aS)-2-[(2R,3R)-3 Cytokine (Mouse) Antibody Cytokine (Rat) Antibody A Th1 Th2 Th17 (Human) Anti

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Development and initial characterization of a novel ghrelin receptor CRISPR/Cas9 knockout wistar rat model.

Ghrelin, a stomach-derived hormone implicated in numerous behaviors including feeding, reward, stress, and addictive behaviors, acts by binding to the growth hormone secretagogue receptor (GHSR). Here, we present the development, verification, and initial characterization of a novel GHSR knockout (KO) Wistar rat model created with CRISPR genome editing.

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CAR,Car,Constitutive andr Androgen Receptor (Phosph Androgen Receptor (Phosph Rabbit Anti-Rat GABA A Re Rabbit Anti-Rat GABA A Re Rabbit Anti-Rat Metabotro Rabbit Anti-Human Androge Rabbit Anti-Human Androge Androgen Receptor (Ab 650 GABA A Receptor a 3 Antib AZD-3514 Mechanisms: Andr Rat(Wistar strain) normal

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Sex-Specific Mechanisms of Resistance Vessel Endothelial Dysfunction Induced by Cardiometabolic Risk Factors.

The incidence of obesity is rising, particularly among women. Microvascular dysfunction is more common with female sex, obesity, and hyperlipidemia and predicts adverse cardiovascular outcomes, but the molecular mechanisms are unclear. Because obesity is associated with mineralocorticoid receptor (MR) activation, we tested the hypothesis that MR in endothelial cells contribute to sex differences in resistance vessel dysfunction in response to cardiometabolic risk factors.

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BYL-719 Mechanisms: PI3K- Lymphatic vessel endothel CAL-101 Mechanisms: PI3K- GSK-2636771 Mechanisms: P IPI-145 (INK-1197) Mechan Actin, Muscle Specific; Actin, Muscle Specific; CD31, Endothelial Cell; CD31, Endothelial Cell; PSA (Prostate Specific A PSA (Prostate Specific A PSAP (Prostate Specific

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