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#33249776   2020/11/28 To Up

Reduced RING finger protein 10 expression in macrophages is associated with aging-related inflammation.

Age-associated decline of the immune system is referred to as immunosenescence. The E3 ligase RING finger 10 (RNF10) has long been associated with the innate immune response, but a potential role in immunosenescence has not previously been reported. In the present study, we identified that RNF10 expression is lower in aged mouse macrophages than in young cells. After lipopolysaccharide (LPS) stimulation, RNF10 expression remained at a basal low level in aged mouse cells, but declined sharply in young mouse cells. Knockdown of RNF10 enhanced both the nuclear factor-κB (NF-κB) and interferon regulatory factor 3 (IRF3) signaling pathways and thus enhanced proinflammatory cytokines and type I interferons (IFN-I) in macrophages, promoting clearance of L. monocytigenes. These findings indicate that dysregulated expression of RNF10 is associated with age-associated immune dysfunction, and RNF10 may thus be a potential target for the treatment of age-related inflammatory diseases.
Xinyuan Cao, Lidan Liu, Yueyi Zhang, Yingyun Yang

2051 related Products with: Reduced RING finger protein 10 expression in macrophages is associated with aging-related inflammation.

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#33249765   2020/11/29 To Up

Time for rethinking the different β-actin transgenic mouse models?

The actin family is crucial for many cellular processes and in mammals muscle and non-muscle forms exist. The latter group contains cytoplasmic-β-actin and cytoplasmic-γ-actin, almost identical in amino acid sequence and with a significant functional overlap. We introduce the properties of the Actb gene and mRNA transcript(s) with main focus on the 3'UTR and its unique features, i.e. the zipcode and two polyadenylation sites creating transcripts of different lengths. Several transgenic mouse models with a modified Actb locus have been created. The different mouse models can be divided into three groups; i.e. 5' or 3' insertion models, mouse models with loxP sequences around exon 2-3 resulting in deletion the start codon, and models with gene edited Actb sequences that produces γ-actin protein instead of β-actin. Whole body knockouts and, with one exception, insertion models lead to embryonic lethality indicating that the Actb gene or transcripts or translated β-actin are essential. Tissue specific ablation at later developmental stages lead to no, or mild phenotypes, suggesting that the Actb gene or β-actin protein is somewhat dispensable. Gene edited Actb mice that produce γ-actin are viable. This assumes that the nucleotide sequence of Actb is important and not the specific amino acid sequence of the protein it encodes. Upregulation of other actin paralogs was frequently observed upon β-actin ablation and can also engage in the phenotype. For a better understanding it will be necessary to analyze in current and future models all relevant actin transcripts and protein levels in a standardized and comprehensive way. This article is protected by copyright. All rights reserved.
Bieke Vanslembrouck, Christophe Ampe, Jolanda van Hengel

1633 related Products with: Time for rethinking the different β-actin transgenic mouse models?

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#33249762   2020/11/28 To Up

Oxidized low-density lipoprotein accelerates the injury of endothelial cells via circ-USP36/miR-98-5p/VCAM1 axis.

Circular RNAs (circRNAs) are a group of RNAs featured by a covalently closed continuous loop structure. This study aimed to uncover the function and mechanism of circ-ubiquitin specific peptidase 36 (USP36) in endothelial cells treated with oxidized low-density lipoprotein (ox-LDL). The levels of circ-USP36, microRNA-98-5p (miR-98-5p) and vascular cell adhesion molecule 1 (VCAM1) were examined by a quantitative real-time polymerase chain reaction (qRT-PCR). The viability, apoptosis and inflammation were detected by (4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, flow cytometry and enzyme-linked immunosorbent assay (ELISA), respectively. Western blot assay was performed to detect the expression of apoptosis and proliferation-related markers and VCAM1 protein level. The targets of circ-USP36 and miR-98-5p were searched using starBase website, and dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were applied to validate the above predictions. Ox-LDL exposure induced the upregulation of circ-USP36 in HUVEC cells. Circ-USP36 accelerated ox-LDL-induced apoptosis, inflammatory and viability inhibition of HUVEC cells. MiR-98-5p was a direct downstream gene of circ-USP36. Circ-USP36 promoted the injury of ox-LDL-induced HUVEC cells through targeting miR-98-5p. VCAM1 could bind to miR-98-5p, and the protective effects of miR-98-5p accumulation on ox-LDL-induced HUVEC cells were reversed by the transfection of VCAM1. VCAM1 was regulated by circ-USP36/miR-98-5p signaling in HUVEC cells. Ox-LDL promoted the apoptosis and inflammation but suppressed the viability of HUVEC cells through upregulating circ-USP36, thus elevating the expression of VCAM1 via miR-98-5p.
Kuang Peng, Peiyong Jiang, Yafang Du, Dianmei Zeng, Junbi Zhao, Meiling Li, Chunchen Xia, Zhong Xie, Jie Wu

1709 related Products with: Oxidized low-density lipoprotein accelerates the injury of endothelial cells via circ-USP36/miR-98-5p/VCAM1 axis.

100ug Lyophilized1.00 flask1.00 flask1.00 flask100ug Lyophilized1.00 flask0.5 ml1 vial1.00 flask100ug Lyophilized1.00 flask1.00 flask

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#33249758   2020/11/28 To Up

Parathyroid hormone ameliorates osteogenesis of human bone marrow mesenchymal stem cells against glucolipotoxicity through p38 MAPK signaling.

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Yuli Wang, Lintong Huang, Ziyue Qin, Hua Yuan, Bing Li, Yongchu Pan, Xiaoqian Wang, Xin Du, Shushu Hao, Yifei Du, Ruixia Wang, Yi Shen

2132 related Products with: Parathyroid hormone ameliorates osteogenesis of human bone marrow mesenchymal stem cells against glucolipotoxicity through p38 MAPK signaling.

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#33249756   2020/11/29 To Up

Luminal polyethylene-glycol solution delays the onset of preservation injury in the human intestine.

The organ damage incurred during the cold storage (CS) of intestinal grafts has short and long-term consequences. Animal studies suggest that additional luminal preservation (LP) with polyethylene-glycol (PEG) may alleviate this damage. This study aims to validate these findings using human intestines. Ileal segments, perfused intravascularly with IGL-1 solution, were procured from 32 multiorgan donors and divided into two parts: one containing a PEG 3350-based solution introduced luminally (LP group) and another one without luminal treatment (control). Sampling was performed after 4h, 8h, 14h, and 24h of CS. Histology was assessed using the Chiu/Park score. Tight junctions (TJ), several inflammatory markers, and transcription factors were examined by immunofluorescence, ddPCR, and Western blot. Tissue water content (edema) was also measured. Apoptotic activity was assessed with caspase 2,3 and 9 assays. LP significantly lowered mucosal injury at all time points. Redistribution of TJ proteins occurred earlier and more severely in the control group. After 24h of CS, LP intestines showed an emerging unfolding protein response. Increased caspase-3 and -9 activity were found in the control group. The current results indicate that luminal PEG is safe and effective in reducing damage to the intestinal epithelium during CS.
John Mackay Søfteland, Jasmine Bagge, Arvind Manikantan Padma, Anna Casselbrant, Changlian Zhu, Yafeng Wang, Mats Hellström, Michael Olausson, Mihai Oltean

2925 related Products with: Luminal polyethylene-glycol solution delays the onset of preservation injury in the human intestine.

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#33249747   2020/11/29 To Up

Interleukin 6 trans-signaling is a critical driver of lung allograft fibrosis.

Histopathologic examination of lungs afflicted by chronic lung allograft dysfunction (CLAD) consistently show both mononuclear cell (MNC) inflammation and mesenchymal cell (MC) fibroproliferation. We hypothesize that interleukin 6 (IL-6) trans-signaling may be a critical mediator of MNC-MC crosstalk and necessary for the pathogenesis of CLAD. Bronchoalveolar lavage (BAL) fluid obtained after the diagnosis of CLAD has approximately 2-fold higher IL-6 and soluble IL-6 receptor (sIL-6R) levels compared to matched pre-CLAD samples. Human BAL-derived MCs do not respond to treatment with IL-6 alone but have rapid and prolonged JAK2-mediated STAT3 Tyr705 phosphorylation when exposed to the combination of IL-6 and sIL-6R. STAT3 phosphorylation within MCs upregulates numerous genes causing increased invasion and fibrotic differentiation. MNC, a key source of both IL-6 and sIL-6R, produce minimal amounts of these proteins at baseline but significantly upregulate production when cocultured with MCs. Finally, the use of an IL-6 deficient recipient in a murine orthotopic transplant model of CLAD reduces allograft fibrosis by over 50%. Taken together these results support a mechanism where infiltrating MNCs are stimulated by resident MCs to release large quantities of IL-6 and sIL-6R which then feedback onto the MCs to increase invasion and fibrotic differentiation.
David S Wheeler, Keizo Misumi, Natalie M Walker, Ragini Vittal, Michael P Combs, Yoshiro Aoki, Russell R Braeuer, Vibha N Lama

1790 related Products with: Interleukin 6 trans-signaling is a critical driver of lung allograft fibrosis.

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#33249724   2020/11/29 To Up

Serum YKL-40 and IL 17 in Psoriasis: Reliability as Prognostic Markers for Disease severity and Responsiveness to treatment.

YKL-40, a mammalian chitinase 3- like protein that was associated with multiple inflammatory and immune diseases. Previous studies have suggested a role for YKL-40 in psoriasis based on its significantly higher levels in the serum of psoriatic patient compared to healthy controls.
S A Khashaba, E M Attwa, N M Said, S Ahmed, F Khattab

2763 related Products with: Serum YKL-40 and IL 17 in Psoriasis: Reliability as Prognostic Markers for Disease severity and Responsiveness to treatment.

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#33249717   2020/11/29 To Up

Insight into the hypercoagulable state of high-risk thrombotic APS patients: Contribution of aβ2GPI and aPS/PT antibodies.

Most high-risk thrombotic Antiphospholipid Syndrome (APS) patients test positive for anti-β2-Glycoprotein I (aβ2GPI) and anti-Phosphatidylserine/Prothrombin (aPS/PT) antibodies. Information on the influence of these antibodies on thrombin generation and activated protein C resistance (aPCr) is still sparse and contradictory.
Elena Pontara, Maria Grazia Cattini, Chunyan Cheng, Elisa Bison, Gentian Denas, Vittorio Pengo

2964 related Products with: Insight into the hypercoagulable state of high-risk thrombotic APS patients: Contribution of aβ2GPI and aPS/PT antibodies.

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#33249714   2020/11/29 To Up

Which Inflammatory Marker is more reliable in Diagnosing Acute Septic Arthritis in Pediatric Population?

The present study aimed to investigate the levels of C-reactive protein (CRP), white blood cell (WBC), erythrocyte sedimentation rate (ESR), neutrophil to lymphocyte ratio (NLR), and platelet to lymphocyte ratio (PLR) as possible indirect inflammatory markers in children with septic arthritis (SA) for diagnosis.
Serkan Bayram, Fuat Bilgili, Doğan Kiral, Taha Furkan Yağci, Ahmet Müçteba Yildirim, Mehmet Demirel

1962 related Products with: Which Inflammatory Marker is more reliable in Diagnosing Acute Septic Arthritis in Pediatric Population?

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#33249703   2020/11/29 To Up

ADFP promotes cell proliferation in lung adenocarcinoma via Akt phosphorylation.

Previously, we identified differentially expressed proteins, including ADFP, between lung adenocarcinoma (LAC) tissue and paired normal bronchioloalveolar epithelium. In this study, we investigated the role of ADFP in LAC. ADFP levels in the serum of patients with lung cancer and benign diseases were measured by enzyme-linked immunosorbent assays (ELISA). shRNA was used to knock-down or overexpress ADFP in A549 and NCI-H1299 cells. The biological function of ADFP and its underlying mechanisms was evaluated in vivo and in vitro. ADFP was highly expressed in the serum of lung cancer patients, especially those with LAC. ADFP promoted cell proliferation and up-regulated the p-Akt/Akt ratio in A549 and NCI-H1299 cells in vitro. Furthermore, in nude mice, ADFP promoted tumour formation with high levels of p-Akt/Akt, Ki67 and proliferating cell nuclear antigen (PCNA). Similar to the effect of ADFP knock-down, MK-2206 (a phosphorylation inhibitor of Akt) reduced A549 and NCI-H1299 cell proliferation. In ADFP-overexpressing A549 and NCI-H1299 cells, proliferation was suppressed by MK-2206 and returned to the control level. ADFP did not regulate invasion, migration or adhesion in LAC cells. Together, these results suggest that ADFP promotes LAC cell proliferation in vitro and in vivo by increasing Akt phosphorylation level.
Xia Meng, Ruiying Sun, Wei Wang, Na Zhang, Shiguang Cao, Boxuan Liu, Ping Fang, Shanshan Deng, Shuanying Yang

1789 related Products with: ADFP promotes cell proliferation in lung adenocarcinoma via Akt phosphorylation.

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