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#28992627   2017/10/09 Save this To Up

H3 Relaxin Protects Against Myocardial Injury in Experimental Diabetic Cardiomyopathy by Inhibiting Myocardial Apoptosis, Fibrosis and Inflammation.

Apoptosis, fibrosis and NLRP3 inflammasome activation are involved in the development of diabetic cardiomyopathy (DCM). Human recombinant relaxin-3 (H3 relaxin) is a novel bioactive peptide that inhibits cardiac injury; however, whether H3 relaxin prevents cardiac injury in rats with DCM and the underlying mechanisms are unknown.

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Influenza A H3N2 Viral Ly Rabbit Anti-Influenza-A H Rabbit Anti-Influenza-A H Rabbit Anti-Influenza-A H Mouse Anti-Influenza-A HA Mouse Anti-Influenza-A He Mouse Anti-Influenza-A He Native Influenza A Virus Native Influenza A Virus Native Influenza A Virus Recombinant Influenza A V Recombinant Influenza A V

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#28718726   2017/07/18 Save this To Up

Effects of the Notch1 signaling pathway on human lung cancer A549 cells.

To evaluate the effects of the Notch1 signaling pathway on human lung cancer A549 cells.

1270 related Products with: Effects of the Notch1 signaling pathway on human lung cancer A549 cells.

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#28435271   2017/04/24 Save this To Up

Recombinant human brain-derived neurotrophic factor prevents neuronal apoptosis in a novel in vitro model of subarachnoid hemorrhage.

Subarachnoid hemorrhage (SAH) is a hemorrhagic stroke with high mortality and morbidity. An animal model for SAH was established by directly injecting a hemolysate into the subarachnoid space of rats or mice. However, the in vitro applications of the hemolysate SAH model have not been reported, and the mechanisms remain unclear. In this study, we established an in vitro SAH model by treating cortical pyramidal neurons with hemolysate. Using this model, we assessed the effects of recombinant human brain-derived neurotrophic factor (rhBDNF) on hemolysate-induced cell death and related mechanisms. Cortical neurons were treated with 10 ng/mL or 100 ng/mL rhBDNF prior to application of hemolysate. Hemolysate treatment markedly increased cell loss, triggered apoptosis, and promoted the expression of caspase-8, caspase-9, and cleaved caspase-3. rhBDNF significantly inhibited hemolysate-induced cell loss, neuronal apoptosis, and expression of caspase-8, caspase-9, and cleaved caspase-3. Our data revealed a previously unrecognized protective activity of rhBDNF against hemolysate-induced cell death, potentially via regulation of caspase-9-, caspase-8-, and cleaved caspase-3-related apoptosis. This study implicates that hemolysate-induced cortical neuron death represents an important in vitro model of SAH.

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#28398345   2017/04/11 Save this To Up

Genome-wide target specificities of CRISPR RNA-guided programmable deaminases.

Cas9-linked deaminases, also called base editors, enable targeted mutation of single nucleotides in eukaryotic genomes. However, their off-target activity is largely unknown. Here we modify digested-genome sequencing (Digenome-seq) to assess the specificity of a programmable deaminase composed of a Cas9 nickase (nCas9) and the deaminase APOBEC1 in the human genome. Genomic DNA is treated with the base editor and a mixture of DNA-modifying enzymes in vitro to produce DNA double-strand breaks (DSBs) at uracil-containing sites. Off-target sites are then computationally identified from whole genome sequencing data. Testing seven different single guide RNAs (sgRNAs), we find that the rAPOBEC1-nCas9 base editor is highly specific, inducing cytosine-to-uracil conversions at only 18 ± 9 sites in the human genome for each sgRNA. Digenome-seq is sensitive enough to capture off-target sites with a substitution frequency of 0.1%. Notably, off-target sites of the base editors are often different from those of Cas9 alone, calling for independent assessment of their genome-wide specificities.

1999 related Products with: Genome-wide target specificities of CRISPR RNA-guided programmable deaminases.

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#27988354   2016/12/18 Save this To Up

The anti-tumor effects of the recombinant toxin protein rLj-RGD3 from Lampetra japonica on pancreatic carcinoma Panc-1 cells in nude mice.

Recombinant Lampetra japonica RGD peptide (rLj-RGD3) is a soluble toxin protein with three RGD (Arg-Gly-Asp) motifs and a molecular weight of 13.5kDa. The aim of this study was to investigate the effects and mechanisms of rLj-RGD3 on tumor growth and survival in pancreatic carcinoma Panc-1 cell-bearing mice. A Panc-1 human pancreatic carcinoma-bearing nude mouse model was successfully generated, and the animals were treated with different doses of rLj-RGD3 for 3 weeks. The volume and weight of the subcutaneous tumors, the survival of the nude mice, histopathological changes, the intratumoral MVD, the number of apoptotic Panc-1 cells, and apoptosis-related proteins and gene expressions were determined. rLj-RGD3 significantly decreased the tumor volumes and weights, and the maximum tumor volume and weight IR values were 53.2% (p<0.001) and 55.9% (p<0.001), respectively. The life expectancy of Panc-1-bearing nude mice treated with rLj-RGD3 was increased by 56.3% (p<0.001). Meanwhile, rLj-RGD3 promoted the expression of Bax, caspase-3, and caspase-9 and inhibited Bcl-2 and VEGF expression. In addition, rLj-RGD3 did not change FAK, PI3K and Akt expression, but p-FAK, p-PI3K and p-Akt, levels were down-regulated. These results show that rLj-RGD3 induced potent anti-tumor activity in vivo and suppressed the growth of transplanted Panc-1 cells in a nude mouse model, implying that rLj-RGD3 may serve as a potent clinical therapeutic agent for human pancreatic carcinoma.

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#27907031   2016/12/01 Save this To Up

In Vitro Pre-Clinical Validation of Suicide Gene Modified Anti-CD33 Redirected Chimeric Antigen Receptor T-Cells for Acute Myeloid Leukemia.

Approximately fifty percent of patients with acute myeloid leukemia can be cured with current therapeutic strategies which include, standard dose chemotherapy for patients at standard risk of relapse as assessed by cytogenetic and molecular analysis, or high-dose chemotherapy with allogeneic hematopoietic stem cell transplant for high-risk patients. Despite allogeneic hematopoietic stem cell transplant about 25% of patients still succumb to disease relapse, therefore, novel strategies are needed to improve the outcome of patients with acute myeloid leukemia.

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#27865841   2016/11/20 Save this To Up

Survivin does not influence the anti-apoptotic action of XIAP on caspase-9.

Survivin inhibits apoptosis in numerous tumor cell lines and has emerged as promising target for cancer therapy. The anti-apoptotic effect of survivin was attributed to a direct interaction with XIAP (X-linked inhibitor of apoptosis) and to an indirect effect, where survivin antagonizes the anti-XIAP action of Smac. The direct interaction is thought to lead to synergistic inhibition of caspase-9 and, at the same time, to enhanced stability of XIAP by reducing its auto-ubiquitination. Using recombinant proteins, we have investigated the influence of survivin on the inhibition of caspase-9 by XIAP in vitro. With a fluorescence-based assay for the apoptosome-stimulated activity of caspase-9, we show that survivin has no effect on the inhibition of caspase-9 by XIAP, neither in the presence nor in the absence of Smac. Employing analytical size exclusion chromatography (SEC) and analytical ultracentrifugation, we show that survivin does not physically interact with XIAP. We confirm in vitro that XIAP ubiquitinates itself in the presence of the appropriate recombinant enzymes and Mg(2+)-ATP and could show that survivin neither influences the kinetics nor the extent of XIAP's self-ubiquitination. Our results call for a revision of the current view of how survivin interferes with the mitochondrial pathway of apoptosis.

2731 related Products with: Survivin does not influence the anti-apoptotic action of XIAP on caspase-9.

Rabbit Anti-Caspase-7 (CA Rabbit Anti-Human Survivi Rabbit Anti-Human Survivi Rabbit Anti-Human Survivi Rabbit Anti-Human XIAP An Rabbit Anti-Human XIAP An Rabbit Anti-Human XIAP (+ Anti-Cleaved-Caspase-3 PC Anti Cleaved Caspase 3 PC Anti-Cleaved-Caspase-3 PC Anti Cleaved Caspase 3 PC Rabbit anti PKC theta (Ab

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#27034262   2016/04/01 Save this To Up

The roles of serum PDCD5 in circulating CD133 positive cells of the patients with gastric cancer.

Cancer stem cells are responsible for the development, metastasis, recurrence, and drug resistance of cancer. More and more studies exhibited that the circulating CD133(+) cells is a marker for the prognosis of various malignancies. Programmed cell death protein 5 (PDCD5) can promote apoptosis in different tumor cell types in response to various stimuli. However, the impact of PDCD5 on circulating CD133(+) cells of gastric cancer patients remains unclear. In this study, we detected serum PDCD5 level in blood samples of the patients with gastric cancer by using ELISA. MTT assay, sphere assay, and wound healing assay were used to test the anti-tumor effects of rhPDCD5 on CD133(+) cells in vitro. Lower serum levels of PDCD5 protein were identified in the gastric cancer patients that with CD133(+) fraction more than 1.6 %. No difference between healthy controls and the gastric cancer patients that with CD133(+) fraction less than 1.6 %. Serum PDCD5 was correlated with the favorable prognosis of patients with gastric cancer. In the last, we confirmed that rhPDCD5 could induce apoptosis, and inhibit the proliferation, colony formation, and mobility of CD133(+) cells in vitro by suppressing MEK/ERK pathway. Serum PDCD5 could be considered as a potential drug for the gastric cancer patients with circulating CD133(+) cells.

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#27764084   2016/10/20 Save this To Up

Novel Nuclear Factor-KappaB Targeting Peptide Suppresses β-Amyloid Induced Inflammatory and Apoptotic Responses in Neuronal Cells.

In the central nervous system (CNS), activation of the transcription factor nuclear factor-kappa B (NF-κβ) is associated with both neuronal survival and increased vulnerability to apoptosis. The mechanisms underlying these dichotomous effects are attributed to the composition of NF-κΒ dimers. In Alzheimer's disease (AD), β-amyloid (Aβ) and other aggregates upregulate activation of p65:p50 dimers in CNS cells and enhance transactivation of pathological mediators that cause neuroinflammation and neurodegeneration. Hence selective targeting of activated p65 is an attractive therapeutic strategy for AD. Here we report the design, structural and functional characterization of peptide analogs of a p65 interacting protein, the glucocorticoid induced leucine zipper (GILZ). By virtue of binding the transactivation domain of p65 exposed after release from the inhibitory IκΒ proteins in activated cells, the GILZ analogs can act as highly selective inhibitors of activated p65 with minimal potential for off-target effects.

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#27548616   2016/08/23 Save this To Up

Redirecting Specificity of T cells Using the Sleeping Beauty System to Express Chimeric Antigen Receptors by Mix-and-Matching of VL and VH Domains Targeting CD123+ Tumors.

Adoptive immunotherapy infusing T cells with engineered specificity for CD19 expressed on B- cell malignancies is generating enthusiasm to extend this approach to other hematological malignancies, such as acute myelogenous leukemia (AML). CD123, or interleukin 3 receptor alpha, is overexpressed on most AML and some lymphoid malignancies, such as acute lymphocytic leukemia (ALL), and has been an effective target for T cells expressing chimeric antigen receptors (CARs). The prototypical CAR encodes a VH and VL from one monoclonal antibody (mAb), coupled to a transmembrane domain and one or more cytoplasmic signaling domains. Previous studies showed that treatment of an experimental AML model with CD123-specific CAR T cells was therapeutic, but at the cost of impaired myelopoiesis, highlighting the need for systems to define the antigen threshold for CAR recognition. Here, we show that CARs can be engineered using VH and VL chains derived from different CD123-specific mAbs to generate a panel of CAR+ T cells. While all CARs exhibited specificity to CD123, one VH and VL combination had reduced lysis of normal hematopoietic stem cells. This CAR's in vivo anti-tumor activity was similar whether signaling occurred via chimeric CD28 or CD137, prolonging survival in both AML and ALL models. Co-expression of inducible caspase 9 eliminated CAR+ T cells. These data help support the use of CD123-specific CARs for treatment of CD123+ hematologic malignancies.

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