Search results for: Human Epidermal Growth Factor EGF
#32601248 2020/06/29 To Up
Soluble SORLA enhances neurite outgrowth and regeneration through activation of the EGF Receptor/ERK signaling axis.SORLA is a transmembrane trafficking protein associated with Alzheimer's disease (AD) risk. Although SORLA is abundantly expressed in neurons, physiological roles for SORLA remain unclear. Here, we show that cultured transgenic neurons overexpressing SORLA feature longer neurites, and accelerated neurite regeneration with wounding. Enhanced release of a soluble form of SORLA (sSORLA) is observed in transgenic mouse neurons overexpressing human SORLA, while purified sSORLA promotes neurite extension and regeneration. Phosphoproteomic analyses demonstrate enrichment of phosphoproteins related to the epidermal growth factor (EGFR)/ERK pathway in SORLA transgenic mouse hippocampus from both genders. sSORLA co-precipitates with EGFR , and sSORLA treatment increases EGFR Y1173 phosphorylation, which is involved in ERK activation in cultured neurons. Furthermore, sSORLA triggers ERK activation, whereas pharmacological EGFR or ERK inhibition reverses sSORLA-dependent enhancement of neurite outgrowth. In search for downstream ERK effectors activated by sSORLA, we identified upregulation of Fos expression in hippocampus from male mice overexpressing SORLA by RNAseq analysis. We also found that Fos is upregulated and translocates to the nucleus in an ERK-dependent manner in neurons treated with sSORLA. Together, these results demonstrate that sSORLA is an EGFR-interacting protein that activates EGFR/ERK/Fos signaling to enhance neurite outgrowth and regeneration.SORLA is a transmembrane trafficking protein previously known to reduce the levels of amyloid-β, which is critical in the pathogenesis of Alzheimer's disease. In addition, SORLA mutations are a risk factor for Alzheimer's disease. Interestingly, the SORLA ectodomain is cleaved into a soluble form, sSORLA, which has been shown to regulate cytoskeletal signaling pathways and cell motility in cells outside the nervous system. We show here that sSORLA binds and activates the EGF receptor to induce downstream signaling through the ERK serine/threonine kinase and the Fos transcription factor, thereby enhancing neurite outgrowth. These findings reveal a novel role for sSORLA in promoting neurite regeneration through the EGF receptor/ERK/Fos pathway, thereby demonstrating a potential neuroprotective mechanism involving SORLA.
Jessica Stupack, Xiao-Peng Xiong, Lu-Lin Jiang, Tongmei Zhang, Lisa Zhou, Alex Campos, Barbara Ranscht, William Mobley, Elena B Pasquale, Huaxi Xu, Timothy Y Huang
2582 related Products with: Soluble SORLA enhances neurite outgrowth and regeneration through activation of the EGF Receptor/ERK signaling axis.96tests200 200ug100ul100ug100ug0.1 mg1mg200ul100ul1000
#32595893 2020/04/18 To Up
Tensile strength, growth factor content and proliferation activities for two platelet concentrates of platelet-rich fibrin and concentrated growth factor.Platelet-rich fibrin (PRF) can be obtained by centrifuging fresh blood in the absence of anticoagulants. Varying the centrifugation speeds may produce tougher and richer concentrated growth factors (CGF). This study examines tensile strength, growth factor content, and the potential of CGF and PRF in promoting periodontal cell proliferation.
Hung-Maan Lee, E-Chin Shen, John T Shen, Earl Fu, Hsien-Chung Chiu, Yi-Jan Hsia
2904 related Products with: Tensile strength, growth factor content and proliferation activities for two platelet concentrates of platelet-rich fibrin and concentrated growth factor.2ug12ug2ug2ug100 µg1012ug10 µg5 x 50 ug20 ug
#32593399 2020/06/05 To Up
HER family in cancer progression: From discovery to 2020 and beyond.The human epidermal growth factor receptor (HER) family of receptor tyrosine kinases (RTKs) are among the first layer of molecules that receive, interpret, and transduce signals leading to distinct cancer cell phenotypes. Since the discovery of the tooth-lid factor-later characterized as the epidermal growth factor (EGF)-and its high-affinity binding EGF receptor, HER kinases have emerged as one of the commonly upregulated or hyperactivated or mutated kinases in epithelial tumors, thus allowing HER1-3 family members to regulate several hallmarks of cancer development and progression. Each member of the HER family exhibits shared and unique structural features to engage multiple receptor activation modes, leading to a range of overlapping and distinct phenotypes. EGFR, the founding HER family member, provided the roadmap for the development of the cell surface RTK-directed targeted cancer therapy by serving as a prototype/precursor for the currently used HER-directed cancer drugs. We herein provide a brief account of the discoveries, defining moments, and historical context of the HER family and guidepost advances in basic, translational, and clinical research that solidified a prominent position of the HER family in cancer research and treatment. We also discuss the significance of HER3 pseudokinase in cancer biology; its unique structural features that drive transregulation among HER1-3, leading to a superior proximal signaling response; and potential role of HER3 as a shared effector of acquired therapeutic resistance against diverse oncology drugs. Finally, we also narrate some of the current drawbacks of HER-directed therapies and provide insights into postulated advances in HER biology with extensive implications of these therapies in cancer research and treatment.
Rakesh Kumar, Bijesh George, Marcia R Campbell, Nandini Verma, Aswathy Mary Paul, Cecília Melo-Alvim, Leonor Ribeiro, M Radhakrishna Pillai, Luis Marques da Costa, Mark M Moasser
#32585863 2020/06/23 To Up
Mesenchymal Stem Cell Derived Biocompatible Membrane Vesicles Demonstrate Immunomodulatory Activity Inhibiting Activation and proliferation of Human Mononuclear Cells.Immune-mediated diseases are characterized by abnormal activity of the immune system. The cytochalasin B-induced membrane vesicles (CIMVs) are innovative therapeutic instruments. However, the immunomodulating activity of human mesenchymal stem cell (MSC)-derived CIMVs (CIMVs-MSCs) remains unknown. Therefore, we sought to investigate the immunological properties of CIMVs-MSCs and evaluate their effect on human peripheral blood mononuclear cells (PBMCs). We found that CIMVs-MSCs are primarily uptaken by monocytes and B-cells. Additionally, we demonstrated that CIMVs-MSCs inhibit phytohemagglutinin (PHA)-induced proliferation of PBMCs, with more pronounced effect on T-lymphocytes expansion as compared to that of B-cells. In addition, activation of T-helpers (CD4+CD25+), B-cells (CD19+CD25+), and T-cytotoxic lymphocytes (CD8+CD25+) was also significantly suppressed by CIMVs-MSCs. Additionally, CIMVs-MSCs decreased secretion of epidermal growth factor (EGF) and pro-inflammatory Fractalkine in a population of PBMCs, while the releases of FGF-2, G-CSF, anti-inflammatory GM-CSF, MCP-3, anti-inflammatory MDC, anti-inflammatory IL-12p70, pro-inflammatory IL-1b, and MCP-1 were increased. We analyzed the effect of CIMVs-MSCs on an isolated population of CD4+ and CD8+ T-lymphocytes and demonstrated their different immune response and cytokine secretion. Finally, we observed that no xenogeneic nor allogeneic transplantation of CIMVs induced an immune response in mice. Our data suggest that CIMVs-MSCs have immunosuppressive properties, are potential agents for immunomodulating treatment, and are worthy of further investigation.
Marina O Gomzikova, Sevindzh K Kletukhina, Sirina V Kurbangaleeva, Olga A Neustroeva, Olga S Vasileva, Ekaterina E Garanina, Svetlana F Khaiboullina, Albert A Rizvanov
1212 related Products with: Mesenchymal Stem Cell Derived Biocompatible Membrane Vesicles Demonstrate Immunomodulatory Activity Inhibiting Activation and proliferation of Human Mononuclear Cells.1 mg50 ug10 ug15 x 10A5 cells/vial1.00 flask4 X 250 ml.1.00 flask5 x 50 ug4 x 96-well plate1mg
#32558183 2020/06/18 To Up
Senescent Cholangiocytes Release Extracellular Vesicles that Alter Target Cell Phenotype Via the Epidermal Growth Factor Receptor.Primary sclerosing cholangitis (PSC) is a chronic liver disease characterized by peribiliary inflammation and fibrosis. Cholangiocyte senescence is a prominent feature of PSC. Here we hypothesize that extracellular vesicles (EVs) from senescent cholangiocytes influence the phenotype of target cells.
Mohammed S Al Suraih, Christy E Trussoni, Patrick L Splinter, Nicholas F LaRusso, Steven P O'Hara
2299 related Products with: Senescent Cholangiocytes Release Extracellular Vesicles that Alter Target Cell Phenotype Via the Epidermal Growth Factor Receptor.50 ug5 x 50 ug5 x 50 ug10.1ml (1mg/ml)0.1 mg0.1ml (1mg/ml)100ug100ug1 kit(96 Wells)2 Pieces/Box
#32542223 2020/06/05 To Up
Hormonal Contribution to Liver Regeneration.An understanding of the molecular basis of liver regeneration will open new horizons for the development of novel therapies for chronic liver failure. Such therapies would solve the drawbacks associated with liver transplant, including the shortage of donor organs, long waitlist time, high medical costs, and lifelong use of immunosuppressive agents. Regeneration after partial hepatectomy has been studied in animal models, particularly fumarylacetoacetate hydrolase-deficient () mice and pigs. The process of regeneration is distinctive, complex, and well coordinated, and it depends on the interplay among several signaling pathways (eg, nuclear factor κβ, Notch, Hippo), cytokines (eg, tumor necrosis factor α, interleukin 6), and growth factors (eg, hepatocyte growth factor, epidermal growth factor, vascular endothelial growth factor), and other components. Furthermore, endocrinal hormones (eg, norepinephrine, growth hormone, insulin, thyroid hormones) also can influence the aforementioned pathways and factors. We believe that these endocrinal hormones are important hepatic mitogens that strongly induce and accelerate hepatocyte proliferation (regeneration) by directly and indirectly triggering the activity of the involved signaling pathways, cytokines, growth factors, and transcription factors. The subsequent induction of cyclins and associated cyclin-dependent kinase complexes allow hepatocytes to enter the cell cycle. In this review article, we comprehensively summarize the current knowledge regarding the roles and mechanisms of these hormones in liver regeneration. Articles used for this review were identified by searching MEDLINE and EMBASE databases from inception through June 1, 2019.
Anan A Abu Rmilah, Wei Zhou, Scott L Nyberg430 Tests / Kit600 Tests / Kit430 tests96T201 ml2 modulesN/A 100 G100 assays
#32531471 2020/06/10 To Up
Post-pubertal Difference in Nigral Dopaminergic Cells Firing in the Schizophrenia Model Prepared by Perinatal Challenges of a Cytokine, EGF.Schizophrenia in humans typically develops during and after adolescence; however, the biological underpinning for the specificity of this onset time window remains to be determined. In the present study, we investigated this knowledge gap using our own animal model for schizophrenia. Rodents and monkeys challenged with a cytokine, epidermal growth factor (EGF), as neonates are known to exhibit various behavioral and cognitive abnormalities at the post-pubertal stage. We used the EGF-challenged mice as an animal model for schizophrenia to evaluate the electrophysiological impact of this modeling on nigral dopamine neurons before and after puberty. In vivo single unit recording revealed that the burst firing of putative dopamine neurons in substantia nigra pars compacta was significantly higher in the post-pubertal stage of the EGF model than in that of control mice; in contrast, this difference was not observed in the pre-pubertal stage. The increase in burst firing was accompanied by a decline in Ca-activated K (I) currents, which influence the firing pattern of dopamine neurons. In vivo local application of the SK channel blocker apamin (80 μM) to the substantia nigra was less effective at increasing burst firing in the EGF model than in control mice, suggesting the pathologic role of the I decrease in this model. Thus, these results suggest that the aberrant post-pubertal hyperactivity of midbrain dopaminergic neurons is associated with the temporal specificity of the behavioral deficit of this model, and support the hypothesis that this dopaminergic aberration could be implicated in the adolescent onset of schizophrenia.
Hisaaki Namba, Hiroyuki Nawa
1880 related Products with: Post-pubertal Difference in Nigral Dopaminergic Cells Firing in the Schizophrenia Model Prepared by Perinatal Challenges of a Cytokine, EGF.4 Arrays/Slide4 Membranes/Box96 assays10 ug4 Membranes/Box4 Arrays/Slide4 Membranes/Box4 Arrays/Slide4 Arrays/Slide
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#32518154 2020/06/09 To Up
ETS variant transcription factor 5 and c-Myc cooperate in derepressing the human telomerase gene promoter via composite Ets/E-box motifs.Human telomerase gene (hTERT) is repressed in most somatic cells. How transcription factors activate the hTERT promoter in its repressive chromatin environment is unknown. Here, we report that the ETS family protein ETS variant transcription factor 5 (ETV5) mediates epidermal growth factor (EGF)-induced hTERT expression in MCF10A cells. This activation required MYC proto-oncogene bHLH transcription factor (c-Myc) and depended on the chromatin state of hTERT promoter. Using chromatinized bacterial artificial chromosome (BAC) reporters in human fibroblasts, we found that ETV5 and c-Myc/MYC-associated factor X (MAX) synergistically activate the hTERT promoter via two identical, but inverted, composite Ets/E-box motifs enclosing the core promoter. Mutations of Ets or E-box sites in either DNA motif abolished the activation and reduced or eliminated the synergism. ETV5 and c-Myc facilitated each other's binding to the hTERT promoter. ETV5 bound to the hTERT promoter in both telomerase-negative and -positive cells, but it activated the repressed hTERT promoter and altered histone modifications only in telomerase-negative cells. The synergistic ETV5/c-Myc activation disappeared when hTERT promoter repression became relieved because of the loss of distal regulatory elements in chimeric human/mouse BAC reporters. Our results suggest that the binding of c-Myc and ETS family proteins to the Ets/E-box motifs derepresses the hTERT promoter by inducing an active promoter configuration, providing a mechanistic insight into hTERT activation during tumorigenesis.
Fan Zhang, Shuwen Wang, Jiyue Zhu
2514 related Products with: ETS variant transcription factor 5 and c-Myc cooperate in derepressing the human telomerase gene promoter via composite Ets/E-box motifs.10 ug100 μg50μg/vial500IU50ug4 Membranes/Box100 2 100 μg500ug1 kit(96 Wells)20ug
#32514271 2020/05/27 To Up
Epidermal growth factor upregulates expression of MUC5AC via TMEM16A, in chronic rhinosinusitis with nasal polyps.Mucus hypersecretion and goblet cell upregulation are common features of chronic rhinosinusitis with nasal polyps (CRSwNP). Although epidermal growth factor (EGF) has been reported to stimulate the expression of MUC5AC, the major macro-molecular constituent of airway mucus, the precise mechanisms underlying the regulation of MUC5AC expression are still not fully understood. The aim of this study therefore was to investigate the role of EGF in regulation of mucin MUC5AC expression and define the involvement of transmembrane protein 16A (TMEM16A) in mediating the EGF-induced mucus overexpression.
Jian Jiao, Tao Zhang, Yu Zhang, Jingyun Li, Min Wang, Ming Wang, Ying Li, Xiangdong Wang, Luo Zhang
2365 related Products with: Epidermal growth factor upregulates expression of MUC5AC via TMEM16A, in chronic rhinosinusitis with nasal polyps.100.00 ug50 ug4 Membranes/BoxProtein1 kit(96 Wells)100.00 ug50 ug2 Pieces/Box100ug1 kit(96 Wells)10ug100.00 ug
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