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MOUSE ANTI HUMAN FIBROBLASTS_EPITHELIAL CELLS RPE

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[#ABS10509] MOUSE ANTI HUMAN FIBROBLASTS_EPITHELIAL CELLS RPE

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ABS10509 | MOUSE ANTI HUMAN FIBROBLASTS_EPITHELIAL CELLS RPE, 100 TESTS
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(1) Loss of HDAC6 alters gut microbiota and worsens obesity.[TOP]

Pubmed ID :30102568
Publication Date : //
Alterations in gut microbiota are known to affect intestinal inflammation and obesity. Antibiotic treatment can affect weight gain by elimination of histone deacetylase (HDAC) inhibitor-producing microbes, which are anti-inflammatory by augmenting regulatory T (T) cells. We asked whether mice that lack HDAC6 and have potent suppressive T cells are protected from microbiota-induced accelerated weight gain. We crossed wild-type and HDAC6-deficient mice and subjected the offspring to perinatal penicillin, inducing weight gain via microbiota disturbance. We observed that male HDAC6-deficient mice were not protected and developed profoundly accelerated weight gain. The antibiotic-exposed HDAC6-deficient mice showed a mixed immune phenotype with increased CD4 and CD8 T-cell activation yet maintained the enhanced T cell-suppressive function phenotype characteristic of HDAC6-deficient mice. 16S rRNA sequencing of mouse fecal samples reveals that their microbiota diverged with time, with HDAC6 deletion altering microbiome composition. On a high-fat diet, HDAC6-deficient mice were depleted in representatives of the S24-7 family and Lactobacillus but enriched with Bacteroides and Parabacteroides; these changes are associated with obesity. Our findings further our understanding of the influence of HDACs on microbiome composition and are important for the development of HDAC6 inhibitors in the treatment of human diseases.-Lieber, A. D., Beier, U. H., Xiao, H., Wilkins, B. J., Jiao, J., Li, X. S., Schugar, R. C., Strauch, C. M., Wang, Z., Brown, J. M., Hazen, S. L., Bokulich, N. A., Ruggles, K. V., Akimova, T., Hancock, W. W., Blaser, M. J. Loss of HDAC6 alters gut microbiota and worsens obesity.

Authors : Lieber Arnon D, Beier Ulf H, Xiao Haiyan, Wilkins Benjamin J, Jiao Jing, Li Xinmin S, Schugar Rebecca C, Strauch Christopher M, Wang Zeneng, Brown J Mark, Hazen Stanley L, Bokulich Nicholas A, Ruggles Kelly V, Akimova Tatiana, Hancock Wayne W, Blaser Martin J,



(2) Evaluation of anticoagulant agents for the treatment of human metapneumovirus infection in mice.[TOP]

Pubmed ID :30102144
Publication Date : //
Thrombin has been demonstrated to be involved in several viral diseases including human metapneumovirus (hMPV) infections. We previously showed that immediate administration of thrombin inhibitor argatroban post-infection protected mice against hMPV disease. This current work aims at determining whether warfarin and heparin, two other anticoagulants inhibiting thrombin formation and activities, may also be used for treatment against hMPV in vivo. We found that immediate injections of argatroban, warfarin or heparin after virus challenge protected mice against hMPV infection, as evidenced by decreased or no mortality, less weight loss, reduced viral load and attenuated inflammation. However, delayed treatments starting 1 day post-infection with argatroban or warfarin almost did not impact the survival whereas delayed treatment with heparin induced an increased mortality during infection. Moreover, these treatments also did not reduce weight loss, viral replication and inflammation. In agreement with these results, thrombin generation was decreased upon immediate anticoagulant treatments but was unaltered upon delayed treatments. Thus, thrombin generation occurs at the onset of hMPV infection and thrombin inhibition may be only useful for the treatment of this disease when initiated in the early stage. In this case, heparin is not recommended because of its reduced efficacy on mortality in infected mice whereas argatroban and warfarin appear as safe and effective drugs for the treatment of hMPV disease. The antiviral and anti-inflammatory effects of argatroban occur via thrombin-dependent pathways whereas the mechanisms by which warfarin exerts its beneficial effects against hMPV infection were not elucidated and need to be further studied.

Authors : Lê Ba Vuong, Jandrot-Perrus Martine, Couture Christian, Checkmahomed Liva, Venable Marie-Christine, Hamelin Marie-Ève, Boivin Guy,



(3) Targeting NEDD8-activating enzyme is a new approach to treat canine diffuse large B-cell lymphoma.[TOP]

Pubmed ID :30101447
Publication Date : //
Canine diffuse large B-cell lymphoma (DLBCL), the most common hematologic malignancy of dogs, is associated with poor overall survival. The lack of conventional chemotherapies with sustainable efficacy warrants investigation of novel therapies. Pevonedistat (MLN4924) is a potent and selective small molecule NEDD8-activating enzyme inhibitor. In human activated B-cell-like (ABC) diffuse large B-cell lymphoma, pevonedistat induces lymphoma cell apoptosis, DNA damage and G1 cell cycle arrest by inhibiting the nuclear factor-κB (NF-κB) pathway. Genomic and transcriptomic studies showed that the NF-κB pathway is deregulated in canine DLBCL. Our results showed that pevonedistat treatment significantly reduces the viability of canine DLBCL cells by inducing G1 cell cycle arrest and apoptosis. Pevonedistat treatment inhibits NF-κB pathway activation and downregulates NF-κB target genes in canine DLBCL. Moreover, administration of pevonedistat to mice bearing canine DLBCL xenograft tumours resulted in tumour regression. Our in vivo and in vitro studies provide justification for future clinical application of pevonedistat as a potential new anti-cancer therapy that may benefit both canine and human species.

Authors : Assumpção A L F V, Lu Z, Marlowe K W, Shaffer K S, Pan X,



(4) (Sw.), DC induces apoptosis and cell cycle arrest in triple negative breast cancer cells: and investigations.[TOP]

Pubmed ID :30100991
Publication Date : //
Plant originated drugs/formulations are extensively prescribed by the physicians as a complementary therapy for treating various human ailments including cancer. In this study leaves methanol extract was prepared and exposed to human breast cancer cell lines i.e. MDA-MB-231 and MCF-7 and human keratinocytes HaCaT as a representative of normal cells. Initially, a series of experiments like cell proliferation, migration, colony formation, cell cycle arrest and inhibition of angiogenesis. After confirmation of the efficient and selective activity against triple negative breast cancer cell line, we further evaluated the possible mechanism of inducing cell death and experiments like detection of reactive oxygen species, caspases and poly (ADP-ribose) polymerase cleavage study and Annexin V assay were performed. We also evaluated anti tumorigenic activity of the leaves by using 4T1 cells (a triple negative mouse origin breast cancer cell line) and BALB/c xenograft mouse model. experiments revealed that methanol extract of leaves possess impressive anti-breast cancer activity more specifically against triple negative breast cancer cells, while the studies demonstrated that leaves extract significantly suppressed the 4T1 induced tumor growth. Present investigations clearly focus the significance of as an important resource for finding novel leads against triple negative breast cancer. The results may also act as a ready reference towards developing based formulation as an alternative and complementary medicine for the management of breast cancer.

Authors : Gurushidhappa Utage Bhimashankar, Shivajirao Patole Milind, Vasudeo Nagvenkar Punam, Shankar Kamble Sonali, Nivarti Gacche Rajesh,



(5) Transcriptome profiling of anti-müllerian hormone treated preantral/small antral mouse ovary follicles.[TOP]

Pubmed ID :30100987
Publication Date : //
The predisposition for the initiation of folliculogenesis in mammals including humans is programmed to start at fetal life and continues until reproductive capacity. The follicles grow from a pool of primordial follicles which retain the major functions in the entire reproductive life of a female. Anti-müllerian hormone (AMH), a glycoprotein belonging to the transforming growth factor-beta family, has an inhibitory effect on ovarian follicle development. The key regulatory target genes in primordial follicle development are of paramount importance in reproductive biology of female. A systems biology method was used to find regulatory genes performing critical role in primordial follicle development. A complete in-depth bioinformatics analysis was performed to investigate the changes in transcriptome of preantral to small antral mouse follicles treated for 12 h and 24 h with two different concentrations; 50 and 200 ng/ml of AMH, and thereby identify candidate genes in time and concentration manner. Firstly, we found differentially expressed genes that were time and concentration dependent in response to AMH. The network analysis of these differentially expressed genes provided new candidate genes and pathways associated with inhibitory action of AMH on the primordial follicle development. To further emphasize the function of AMH, the key identified genes' protein-protein docking was analyzed and found the intracellular and extracellular protein-protein interaction. This study elucidates one of the novel mechanisms of AMH involvement in inhibition of ovarian follicle development which may lead to prolong productive life in female.

Authors : Ur Rehman Zia, Khan Faheem Ahmad, Farmanullah , Talpur Hira Sajjad, Liu Qing, Liu Shenhe, Yang Liguo,



(6) Emodin and Its Combination with Cytarabine Induce Apoptosis in Resistant Acute Myeloid Leukemia Cells in Vitro and in Vivo.[TOP]

Pubmed ID :30099447
Publication Date : //
Acute myeloid leukemia (AML) remains a hematologic malignancy with poor survival and a high risk of relapse, which is mainly caused by the emergence of multidrug resistance (MDR). The identification of novel agents to improve therapeutic strategies becomes important priority for AML treatment. It has been shown that emodin has therapeutic effects on many kinds of human malignant tumors. In this study, we investigated the anti-leukemia effects of emodin alone or in combination with cytarabine (Ara-C) on multidrug-resistant AML HL-60/ADR cells and in a mouse xenograft model of human highly tumorigenic AML HL-60/H3 cells. The underlying mechanism was also addressed.

Authors : Chen Yingyu, Gan Donghui, Huang Qinghua, Luo Xiaofeng, Lin Donghong, Hu Jianda,



(7) Size-Dependent Neutralizing Activity of Gold Nanoparticle-Based Subunit Vaccine Against Dengue Virus.[TOP]

Pubmed ID :30099200
Publication Date : //
Dengue results in substantial human morbidity and significant socio-economic impacts, but a specific dengue therapeutic is not available. The currently available dengue vaccine has low efficacy and high rate of adverse effects, necessitating different strategies for the development of a safer and more efficient vaccine against dengue virus. We describe here a hybrid combination of different-sized gold nanoparticles (AuNPs) and domain III of envelope glycoprotein derived from serotype 2 of dengue virus (EDIII) as dengue subunit vaccine. The efficacy of the EDIII-functionalized AuNPs (AuNP-E) to induce neutralizing antibody in BALB/c mice is evaluated. Obtained results show that AuNP-E induced a high level of antibody which mediates serotype-specific neutralization of dengue virus. More importantly, the level of antibody is dependent on both the size of AuNPs and the concentration of AuNP-E, implicating the possibility to modulate it through adjusting these parameters. These results represent an important step towards the development of tetravalent AuNP-based subunit dengue vaccine.

Authors : Quach Quang Huy, Ang Swee Kim, Chu Jang-Hann Justin, Kah James Chen Yong,



(8) Combined Inactivation of TP53 and MIR34A Promotes Colorectal Cancer Development and Progression in Mice via Increasing Levels of IL6R and PAI1.[TOP]

Pubmed ID :30099074
Publication Date : //
Combined inactivation of the microRNA 34a gene (MIR34A, by methylation) and the TP53 gene (by mutation or deletion) is observed in 50% of colorectal tumors that progress to distant metastases. We studied mice with intestinal disruption of Mir34a and Tp53 to investigate mechanisms of colorectal carcinogenesis and identify strategies to block these processes.

Authors : Öner Meryem Gülfem, Rokavec Matjaz, Kaller Markus, Bouznad Nassim, Horst David, Kirchner Thomas, Hermeking Heiko,



(9) MicroRNA-124 Dysregulation is Associated With Retinal Inflammation and Photoreceptor Death in the Degenerating Retina.[TOP]

Pubmed ID :30098196
Publication Date : //
We sought to determine the role and retinal cellular location of microRNA-124 (miR-124) in a neuroinflammatory model of retinal degeneration. Further, we explored the anti-inflammatory relationship of miR-124 with a predicted messenger RNA (mRNA) binding partner, chemokine (C-C motif) ligand 2 (Ccl2), which is crucially involved in inflammatory cell recruitment in the damaged retina.

Authors : Chu-Tan Joshua A, Rutar Matt, Saxena Kartik, Aggio-Bruce Riemke, Essex Rohan W, Valter Krisztina, Jiao Haihan, Fernando Nilisha, Wooff Yvette, Madigan Michele C, Provis Jan, Natoli Riccardo,



(10) DNA primase polypeptide 1 (PRIM1) involves in estrogen-induced breast cancer formation through activation of the G2/M cell cycle checkpoint.[TOP]

Pubmed ID :30097999
Publication Date : //
The DNA primase polypeptide 1 (PRIM1) is responsible for synthesizing small RNA primers for Okazaki fragments generated during discontinuous DNA replication. PRIM1 mRNA expression levels in breast tumor samples were detected by real-time PCR analysis. Xenografted tumor model was established to study the carcinogenic role of PRIM1 and its potential therapeutic applications. The average PRIM1 mRNA (copy number x 10 /μg) expression was 4.7-fold higher in tumors than in normal tissue (*p = 0.005, n = 254). PRIM1 was detected preferentially at a higher level (> 40-fold) in poorly differentiated tumor tissues (n = 46) compared with more highly differentiated tumors tissues (n = 10) (*p = 0.005). Poor overall survival rate was correlated to the estrogen receptor positive (ER+, n=20) patients with higher PRIM1 expression when compare to the ER- (n=10) patients (Chi Square test, p = 0.03,). Stable expression of PRIM1-siRNA in the ER+ BT-474 cells-xenograft tumors significantly reduced tumor volume in SCID mice (*p = 0.005). The anti-tumoral effects of inotilone isolated from Phellinus linteus was tested and had significant effects on the inhibition of PRIM1 protein expression in ER+ breast cancer cells. In vivo study was performed by administering inotilone (10 mg/kg, twice a week for 6 weeks), which resulted in significantly reduced BT-474-xenografted tumor growth volume compared with control (n = 5 per group, *p < 0.05). This study provides evidences for the prognostic effects of PRIM1 with poor overall survival rate in the ER+ patients and will be valuable to test for therapeutic purpose. This article is protected by copyright. All rights reserved.

Authors : Lee Wei-Hwa, Chen Li-Ching, Lee Chia-Jung, Huang Chi-Cheng, Ho Yuan-Soon, Yang Po-Sheng, Ho Chi-Tang, Chang Hang-Lung, Lin I-Hsuan, Chang Hui-Wen, Liu Yun-Ru, Wu Chih-Hsiung, Tu Shih-Hsin,