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Search results for: KITLG

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#33575478   2020/11/26 To Up

Anti-oncogenic activities exhibited by paracrine factors of MSCs can be mediated by modulation of and genes in glioma SCs .

Cancer stem cells (CSCs) use their stemness properties to perpetuate their lineage and survive chemotherapy. Currently cell-based and cell-free therapies are under investigation to develop novel anti-cancer treatment modalities. We designed this study to investigate how cell extracts of mesenchymal stem cells affect the growth of glioma stem cells . Gliospheres were generated from the U87MG cell line and treated with conditioned media of Wharton's jelly and bone marrow mesenchymal stem cells. The effects were investigated at the functional and molecular levels. Our results showed that conditioned media from both types of mesenchymal stem cells changed the morphology of spheres and inhibited the proliferation, invasion, and self-renewal ability of glioma stem cells. At the molecular level, metabolism interruption at oxidative phosphorylation, cell cycle arrest, cell differentiation, and upregulation of the immune response were observed. Furthermore, this effect was mediated by the upregulation of the gene inhibiting the Wnt pathway mediated by growth factor activity and downregulation of the gene activated by growth factor and cytokine activity, inhibiting multiple pathways. We conclude that different types of mesenchymal stem cells possess antitumor properties and their paracrine factors, in combination with anti-immune modalities, can provide practical therapeutic targets for glioblastoma treatment.
Nazneen Aslam, Elham Abusharieh, Duaa Abuarqoub, Dema Ali, Dana Al-Hattab, Suha Wehaibi, Ban Al-Kurdi, Fatima Jamali, Walhan Alshaer, Hanan Jafar, Abdalla S Awidi

1445 related Products with: Anti-oncogenic activities exhibited by paracrine factors of MSCs can be mediated by modulation of and genes in glioma SCs .

200.00 ug100 μg100ug500 100ug Lyophilized100.00 ul100ug Lyophilized

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#33561516   2021/02/06 To Up

Asparanin A inhibits cell migration and invasion in human endometrial cancer via Ras/ERK/MAPK pathway.

Asparanin A (AA), a natural compound present in vegetables and medicinal herbs like Asparagus officinalis L., has been investigated extensively for its pharmacological attributes. So far, the effect of AA on endometrial cancer (EC) cell migration and invasion has not been explored. Herein, we elucidated the anti-metastasis mechanism of AA on Ishikawa cells based on miRNA-seq and mRNA-seq integrated analyses. AA treatment led to altered miRNAs expression in Ishikawa cells and inhibited the cell wound healing, cell migration and invasion. Gene Ontology and KEGG enrichment analyses showed that the target genes of different expression miRNAs were significantly enriched in Ras, Rap1 and MAPK signaling pathways. Further verification of these changes via qRT-PCR and Western blot assays in vitro and in vivo demonstrated that AA could suppress human EC cell migration and invasion through Ras/ERK/MAPK pathway. Furthermore, top two miRNAs (miR-6236-p5 and miR-12136_R+8) and top three target genes (KITLG, PDGFD, and NRAS) were identified as functional hub miRNAs and genes through miRNA-target gene network analysis. Our data presented a holistic approach to comprehend the anti-metastatic role of AA in EC after in vitro and in vivo analyses.
Fan Zhang, Zhi-Jing Ni, Lei Ye, Yuan-Yuan Zhang, Kiran Thakur, Carlos L Cespedes-Acuña, Jinzhi Han, Jian-Guo Zhang, Zhao-Jun Wei

1566 related Products with: Asparanin A inhibits cell migration and invasion in human endometrial cancer via Ras/ERK/MAPK pathway.

100 μg2 Pieces/Box96 samples100 μg100 ug/vial100ug Lyophilized24 tests96 samples1.00 flask

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#33558336   2021/02/08 To Up

Germline and somatic genetic variants in the p53 pathway interact to affect cancer risk, progression, and drug response.

Insights into oncogenesis derived from cancer susceptibility loci (single nucleotide polymorphisms, SNP) hold the potential to facilitate better cancer management and treatment through precision oncology. However, therapeutic insights have thus far been limited by our current lack of understanding regarding both interactions of these loci with somatic cancer driver mutations and their influence on tumorigenesis. For example, while both germline and somatic genetic variation to the p53 tumor suppressor pathway are known to promote tumorigenesis, little is known about the extent to which such variants cooperate to alter pathway activity. Here we hypothesize that cancer risk-associated germline variants interact with somatic TP53 mutational status to modify cancer risk, progression, and response to therapy. Focusing on a cancer risk SNP (rs78378222) with a well-documented ability to directly influence p53 activity as well as integration of germline datasets relating to cancer susceptibility with tumor data capturing somatically-acquired genetic variation provided supportive evidence for this hypothesis. Integration of germline and somatic genetic data enabled identification of a novel entry point for therapeutic manipulation of p53 activities. A cluster of cancer risk SNPs resulted in increased expression of pro-survival p53 target gene KITLG and attenuation of p53-mediated responses to genotoxic therapies, which were reversed by pharmacological inhibition of the pro-survival c-KIT signal. Together, our results offer evidence of how cancer susceptibility SNPs can interact with cancer driver genes to affect cancer progression and identify novel combinatorial therapies.
Ping Zhang, Isaac Kitchen-Smith, Lingyun Xiong, Giovanni Stracquadanio, Katherine Brown, Philipp Harald Richter, Marsha D Wallace, Elisabeth Bond, Natasha Sahgal, Samantha Moore, Svanhild Nornes, Sarah De Val, Mirvat Surakhy, David Sims, Xuting Wang, Douglas A Bell, Jorge Zeron-Medina, Yanyan Jiang, Anderson J Ryan, Joanna L Selfe, Janet Shipley, Siddhartha Kar, Paul D P Pharoah, Chey Loveday, Rick Jansen, Lukasz F Grochola, Claire Palles, Andrew Protheroe, Val Millar, Daniel V Ebner, Meghana Pagadala, Sarah P Blagden, Timothy Stanley Maughan, Enric Domingo, Ian Tomlinson, Clare Turnbull, Hannah Carter, Gareth L Bond

1165 related Products with: Germline and somatic genetic variants in the p53 pathway interact to affect cancer risk, progression, and drug response.

100 2 Pieces/Box

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#33475207   2021/01/21 To Up

Differential expression and prediction of function of lncRNAs in the ovaries of low and high fecundity Hanper sheep.

Litter size is an important trait that determines the production efficiency of sheep bred for meat. Its detailed investigation can reveal the molecular mechanisms that control the fecundity of sheep and possibly accelerate the breeding process of new varieties of sheep that have high prolificacy. Long non-coding RNAs (lncRNAs) have proven to be an important factor in the regulation of follicular development. However, the mechanisms by which lncRNAs regulate litter size in sheep remain unclear. In the present study, ovarian tissues from the follicular (F) or luteal phase (L) of Hanper sheep that were either monotocous (M) or polytocous (P; FM, FP, LM and LP groups) were collected and sequenced to identify differentially expressed lncRNAs and predict their function. The results indicate that the number of up- and down-regulated lncRNAs in the follicular phase (FM vs. FP) was 95 and 111 and 109 and 49, respectively, in the luteal phase (LM vs. LP). The functional enrichment of the different lncRNAs coexpressed with mRNA was analysed. The results demonstrated that the KISS1-GnRH-LH/FSH-E2 and EGF-EGFR-RAS-PI3K signalling pathways promoted the initiation of the primordial period, follicular development and ovulation in the follicular phase (FM vs. FP). During the luteal phase (LM vs. LP), the production and development of the corpus luteum in ewes was influenced by the KITLG-KIT/FGF-FGFR/HGF-MET-RAS-ERK signalling pathway. STEM clustering functional enrichment analysis of the differentially expressed lncRNAs indicated that profile11 was principally enriched in the Cytokine-Jak-STAT, PDGF-PDGFR-PI3K and KITLG-KIT-RAS-ERK signalling pathways. By analysis of the differential expression of the lncRNAs and their expression in each group, lncRNAs Xist (loc101112291) and Gtl2 (loc101123329) were found to be highly expressed, suggesting that regulation of follicular development was mediated through methylation processes.
Aiju Liu, Menghe Liu, Yuexin Li, Xiaoyong Chen, Limeng Zhang, Shujun Tian

2441 related Products with: Differential expression and prediction of function of lncRNAs in the ovaries of low and high fecundity Hanper sheep.

5 G4 Membranes/Box25 mg2 Pieces/Box4 Membranes/Box 5 G2 Pieces/Box 5 G4 Arrays/Slide50 ug

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#33407466   2021/01/06 To Up

Identification of a novel mutation in the KITLG gene in a Chinese family with familial progressive hyper- and hypopigmentation.

Familial progressive hyper- and hypopigmentation (FPHH, MIM 145250) is a rare hereditary skin disorder that is predominantly characterized by progressive, diffuse, partly blotchy hyperpigmented lesions intermingled with scattered hypopigmented spots, lentigines and sometimes Cafe-au-lait spots (CALs). Heterozygous mutations of the KIT ligand (KITLG, MIM 184745) gene are responsible for FPHH. To date, only eight KITLG mutations have been reported to be associated with FPHH, and no clear genotype-phenotype correlations have been established. This study aimed to identify the causative mutations in the KITLG gene in two Chinese FPHH patients.
Jianbo Wang, Weisheng Li, Naihui Zhou, Jingliu Liu, Shoumin Zhang, Xueli Li, Zhenlu Li, Ziliang Yang, Miao Sun, Min Li

2448 related Products with: Identification of a novel mutation in the KITLG gene in a Chinese family with familial progressive hyper- and hypopigmentation.

100 20 1 Set300 units12 Pieces/Box

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#33383491   2020/12/16 To Up

Pathology of macrophage activation syndrome in humanized NSGS mice.

"Humanized" immunodeficient mice generated via the transplantation of CD34+ human hematopoietic stem cells (hHSC) are an important preclinical model system. The triple transgenic NOD.Cg-PrkdcIl2rg Tg(CMV-IL3,CSF2,KITLG)1Eav/MloySzJ (NSGS) mouse line is increasingly used as recipient for CD34+ hHSC engraftment. NSGS mice combine the features of the highly immunodeficient NSG mice with transgenic expression of the human myeloid stimulatory cytokines GM-CSF, IL-3, and Kit ligand. While generating humanized NSGS (huNSGS) mice from two independent cohorts, we encountered a fatal macrophage activation syndrome (MAS)-like phenotype resulting from the transplantation of CD34+ hHSC. huNSGS mice exhibiting this phenotype declined clinically starting at approximately 10 weeks following CD34+ hHSC engraftment, with all mice requiring euthanasia by 16 weeks. Gross changes comprised small, irregular liver, splenomegaly, cardiomegaly, and generalized pallor. Hematological abnormalities included severe thrombocytopenia and anemia. Pathologically, huNSGS spontaneously developed a disseminated histiocytosis with infiltrates of activated macrophages and hemophagocytosis predominantly affecting the liver, spleen, bone marrow, and pancreas. The infiltrates were chimeric with a mixture of human and mouse macrophages. Immunohistochemistry suggested activation of the inflammasome in both human and murine macrophages. Active Epstein-Barr virus infection was not a feature. Although the affected mice exhibited robust chimerism of the spleen and bone marrow, the phenotype often developed in the face of low chimerism of the peripheral blood. Given the high penetrance and early lethality associated with the MAS-like phenotype here described, we urge caution when considering the use of huNSGS mice for the development of long-term studies.
James C Tarrant, Zev A Binder, Mattia Bugatti, William Vermi, Joost van den Oord, Brona Ranieri, Charles-Antoine Assenmacher, Natalie Hoepp, Donald M O'Rourke, Xiaochuan Shan, Gwenn Danet-Desnoyers, Enrico Radaelli

1155 related Products with: Pathology of macrophage activation syndrome in humanized NSGS mice.



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#33273976   2020/11/18 To Up

Identification of adhesion-associated DNA methylation patterns in the peripheral nervous system.

Schwann cells are unique glial cells in the peripheral nervous system. These cells provide a range of cytokines and nutritional factors to maintain axons and support axonal regeneration. However, little is known concerning adhesion-associated epigenetic changes that occur in Schwann cells after peripheral nerve injury (PNI). In the present study, adhesion-associated DNA methylation biomarkers were assessed between normal and injury peripheral nerve. Specifically, normal Schwann cells (NSCs) and activated Schwann cells (ASCs) were obtained from adult Wistar rats. After the Schwann cells were identified, proliferation and adhesion assays were used to assess differences between NSCs and ASCs. Methylated DNA immunoprecipitation-sequencing and bioinformatics analysis were used to identify and analyze the differentially methylated genes. Reverse transcription-quantitative PCR was performed to assess the expression levels of adhesion-associated genes. In the present study, the proliferation and adhesion assays demonstrated that ASCs had a more robust proliferative activity and adhesion compared with NSCs. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were performed to identify methylation-associated biological processes and signaling pathways. Protein-protein interaction network analysis revealed that Fyn, Efna1, Jak2, Vav3, Flt4, Epha7, Crk, Kitlg, Ctnnb1 and Ptpn11 were potential markers for Schwann cell adhesion. The expression levels of several adhesion-associated genes, such as vinculin, BCAR1 scaffold protein, collagen type XVIII α1 chain and integrin subunit β6, in ASCs were altered compared with those in NSCs. The current study analyzed adhesion-associated DNA methylation patterns of Schwann cells and identified candidate genes that may potentially regulate Schwann cell adhesion in Wistar rats before and after PNI.
Shanhuai Zuo, Guidong Shi, Jianchao Fan, Baoyou Fan, Xiaolei Zhang, Shen Liu, Yan Hao, Zhijian Wei, Xianhu Zhou, Shiqing Feng

1230 related Products with: Identification of adhesion-associated DNA methylation patterns in the peripheral nervous system.

96T100 ug96tests 50 UG

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#33259600   // To Up

Zebrafish Kit ligands cooperate with erythropoietin to promote erythroid cell expansion.

Kit ligand (Kitlg) is pleiotropic cytokine with a prominent role in vertebrate erythropoiesis. Although the role of Kitlg in this process has not been reported in Danio rerio (zebrafish), in the present study we show that its function is evolutionarily conserved. Zebrafish possess 2 copies of Kitlg genes (Kitlga and Kitlgb) as a result of whole-genome duplication. To determine the role of each ligand in zebrafish, we performed a series of ex vivo and in vivo gain- and loss-of-function experiments. First, we tested the biological activity of recombinant Kitlg proteins in suspension culture from zebrafish whole-kidney marrow, and we demonstrate that Kitlga is necessary for expansion of erythroid progenitors ex vivo. To further address the role of kitlga and kitlgb in hematopoietic development in vivo, we performed gain-of-function experiments in zebrafish embryos, showing that both ligands cooperate with erythropoietin (Epo) to promote erythroid cell expansion. Finally, using the kita mutant (kitab5/b5 or sparse), we show that the Kita receptor is crucial for Kitlga/b cooperation with Epo in erythroid cells. In summary, using optimized suspension culture conditions with recombinant cytokines (Epo, Kitlga), we report, for the first time, ex vivo suspension cultures of zebrafish hematopoietic progenitor cells that can serve as an indispensable tool to study normal and aberrant hematopoiesis in zebrafish. Furthermore, we conclude that, although partial functional diversification of Kit ligands has been described in other processes, in erythroid development, both paralogs play a similar role, and their function is evolutionarily conserved.
Jana Oltova, Ondrej Svoboda, Olga Machonova, Petra Svatonova, David Traver, Michal Kolar, Petr Bartunek

1329 related Products with: Zebrafish Kit ligands cooperate with erythropoietin to promote erythroid cell expansion.

1 kit1000050050 assays1 kit10000 tests2 ml430 tests500 tests100 extractions500 assays1 ml

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#33172741   2020/11/07 To Up

Molecular subtypes based on immune-related genes predict the prognosis for hepatocellular carcinoma patients.

Hepatocellular carcinoma (HCC) is a malignancy exhibiting the highest lethality. The present study aimed to identify different immune-related clusters in HCC and a robust tumor gene signature to facilitate the prognosis prediction for HCC patients.
Bo Hu, Xiao-Bo Yang, Xin-Ting Sang

1706 related Products with: Molecular subtypes based on immune-related genes predict the prognosis for hepatocellular carcinoma patients.

96tests 1L

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