Search results for: GRB2
#33655604 2021/03/03 To Up
Exposure to chewing tobacco promotes primary oral squamous cell carcinoma and regional lymph node metastasis by alterations of SDF1α/CXCR4 axis.A high incidence of oral squamous cell carcinoma (OSCC) is observed in South-East Asian countries due to addictions such as chewing tobacco. Local invasion and distant metastases are primary causes of poor prognosis in OSCC. This study aimed to understand the alterations in metastasis biomarkers, such as stromal cell-derived factor-1α (SDF-1 or SDF1α) and its receptor C-X-C chemokine receptor type 4 (CXCR4), in OSCC patient samples that were stratified based on the history of addiction to chewing tobacco. Targeted immunohistochemical staining and Western blotting were performed on primary tumour and metastatic lymph node (LN) tissues in parallel. Overexpression of hepatocyte growth factor (HGF), activated form of its cognate receptor tyrosine kinase, c-Met (p-Met), GRB2-associated-binding protein 1 (Gab1), phospho-protein kinase B (pAkt), nuclear factor kappa B (NF-κB) and cyclooxygenase-2 (COX-2) were observed in primary tumour and metastatic lymph nodes in both chewer and non-chewer cohorts. Variance analysis showed significant positive correlation between them (P < .0001) indicating upregulation of these biomarkers upon ligand-induced activation of c-Met in both tobacco chewers and non-chewers. Significantly higher expressions of SDF1α and CXCR4 were observed in both primary tumours and metastatic lymph nodes of tobacco chewers (P < .0001) and coincided with overexpressed HGF. In contrast, no significant correlation was observed between expression of HGF and that of SDF1α and CXCR4 in non-chewers. Together, our findings provide important insights into the association of HGF/c-Met and the SDF1α/CXCR4 axis in lymph node metastasis and to an aetiological link with the habit of chewing tobacco.
Sudipta Ray, Depanwita Saha, Neyaz Alam, Saunak Mitra Mustafi, Shyamsundar Mandal, Aniruddha Sarkar, Biswanath Majumder, Nabendu Murmu
2801 related Products with: Exposure to chewing tobacco promotes primary oral squamous cell carcinoma and regional lymph node metastasis by alterations of SDF1α/CXCR4 axis.
#33649481 2021/03/01 To Up
Exploration in the mechanism of fucosterol for the treatment of non-small cell lung cancer based on network pharmacology and molecular docking.Fucosterol, a sterol isolated from brown algae, has been demonstrated to have anti-cancer properties. However, the effects and underlying molecular mechanism of fucosterol on non-small cell lung cancer remain to be elucidated. In this study, the corresponding targets of fucosterol were obtained from PharmMapper, and NSCLC related targets were gathered from the GeneCards database, and the candidate targets of fucosterol-treated NSCLC were predicted. The mechanism of fucosterol against NSCLC was identified in DAVID6.8 by enrichment analysis of GO and KEGG, and protein-protein interaction data were collected from STRING database. The hub gene GRB2 was further screened out and verified by molecular docking. Moreover, the relationship of GRB2 expression and immune infiltrates were analyzed by the TIMER database. The results of network pharmacology suggest that fucosterol acts against candidate targets, such as MAPK1, EGFR, GRB2, IGF2, MAPK8, and SRC, which regulate biological processes including negative regulation of the apoptotic process, peptidyl-tyrosine phosphorylation, positive regulation of cell proliferation. The Raf/MEK/ERK signaling pathway initiated by GRB2 showed to be significant in treating NSCLC. In conclusion, our study indicates that fucosterol may suppress NSCLC progression by targeting GRB2 activated the Raf/MEK/ERK signaling pathway, which laying a theoretical foundation for further research and providing scientific support for the development of new drugs.
Xiaoling Li, Baixin Lin, Zhiping Lin, Yucui Ma, Qu Wang, Yushi Zheng, Liao Cui, Hui Luo, Lianxiang Luo
1056 related Products with: Exploration in the mechanism of fucosterol for the treatment of non-small cell lung cancer based on network pharmacology and molecular docking.
#33635226 2021/02/15 To Up
Modulation of miR-548m encoded by X chromosome on the PTEN pathway in systemic lupus erythematosus.Systemic lupus erythematosus (SLE) is a typical autoimmune disease, which is associated with many factors, such as miRNAs. The effect of miRNAs encoded by X chromosome (X-linked miRNAs) plays a crucial role in autoimmune disease. This study aims to identify X-linked miRNAs and validate the pathway influenced by miRNAs in SLE.
Xiaolan Yang, Liyu Shi, Xiaoqiu Zheng, Xinyi Liu, Jun Qian
1027 related Products with: Modulation of miR-548m encoded by X chromosome on the PTEN pathway in systemic lupus erythematosus.1 Set2 Pieces/Box2 Pieces/Box2 Pieces/Box1 Set2 Pieces/Box7 inhibitors2 Pieces/Box2 Pieces/Box
#33634019 2021/02/08 To Up
ECT2 Increases the stability of EGFR and Tumorigenicity by Inhibiting Grb2 Ubiquitination in Pancreatic Cancer.The poor prognosis of patients with pancreatic ductal adenocarcinoma (PDAC) is associated with the invasion and metastasis of tumor cells. Epithelial cell transforming 2 (ECT2) is a guanine nucleotide exchange factor (GEF) of the Rho family of GTPases. It has also been reported that upregulation of ECT2 in pancreatic cancer, but the role and mechanism of ECT2 have not been previously determined. We found that ECT2 was significantly elevated in PDAC tissues and cells, correlated with more advanced AJCC stage, distant metastases, and overall survival of patients with PDAC. Inhibition and overexpression tests showed that ECT2 promoted proliferation, migration and invasion , and promoted tumor growth and metastasis . We determined that ECT2 was involved in the post-translational regulation of Grb2. ECT2 inhibited the degradation of Grb2 through deubiquitination. Furthermore, knockdown of ECT2 downregulated EGFR levels by accelerating EGFR degradation. EGF stimulation facilitated the formation of ECT2-Grb2 complex. Overall, our findings indicated that ECT2 could be used as a promising new therapeutic candidate for PDAC.
Junxiong Wang, Shuo Yang, Li Min, Shengtao Zhu, Shuilong Guo, Shutian Zhang
1692 related Products with: ECT2 Increases the stability of EGFR and Tumorigenicity by Inhibiting Grb2 Ubiquitination in Pancreatic Cancer.
#33629656 2021/02/25 To Up
The SWELL1-LRRC8 complex regulates endothelial AKT-eNOS signaling and vascular function.The endothelium responds to numerous chemical and mechanical factors in regulating vascular tone, blood pressure and blood flow. The endothelial volume regulatory anion channel (VRAC) has been proposed to be mechano-sensitive and thereby sense fluid flow and hydrostatic pressure to regulate vascular function. Here, we show that the Leucine Rich Repeat Containing Protein 8a, LRRC8A (SWELL1) is required for VRAC in human umbilical vein endothelial cells (HUVECs). Endothelial LRRC8A regulates AKT-eNOS signaling under basal, stretch and shear-flow stimulation, forms a GRB2-Cav1-eNOS signaling complex, and is required for endothelial cell alignment to laminar shear flow. Endothelium-restricted KO mice develop hypertension in response to chronic angiotensin-II infusion and exhibit impaired retinal blood flow with both diffuse and focal blood vessel narrowing in the setting of Type 2 diabetes (T2D). These data demonstrate that LRRC8A regulates AKT-eNOS in endothelium and is required for maintaining vascular function, particularly in the setting of T2D.
Ahmad F Alghanem, Javier Abello, Joshua M Maurer, Ashutosh Kumar, Chau My Ta, Susheel K Gunasekar, Urooj Fatima, Chen Kang, Litao Xie, Oluwaseun Adeola, Megan Riker, Macaulay Elliot-Hudson, Rachel A Minerath, Chad E Grueter, Robert F Mullins, Amber N Stratman, Rajan Sah
1012 related Products with: The SWELL1-LRRC8 complex regulates endothelial AKT-eNOS signaling and vascular function.2ug x 202ug2ug2ug2ug2ug5ug96T 6 ml Ready-to-use 1 kit(96 Wells) 25 MG1.00 flask
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#33603781 2021/01/30 To Up
Neuroprotective Effects of ZiBuPiYin Recipe on db/db Mice via PI3K-Akt Signaling Pathway by Activating Grb2.Diabetes-associated cognitive decline (DACD) is one of the nervous system dysfunctions induced by diabetes mellitus with cognitive impairment as the major symptom. In a previous preliminary proteomic study, we found that endoplasmic reticulum processing and PI3K-Akt signaling pathway might be impaired in DACD pathogenesis. In addition, growth factor receptor-bound protein 2 might be a crucial protein as a molecular target of the neuroprotective effects of ZiBuPiYin recipe (ZBPYR).
Wei-Ming Ren, Ze-Bin Weng, Xin Li, Li-Bin Zhan
2258 related Products with: Neuroprotective Effects of ZiBuPiYin Recipe on db/db Mice via PI3K-Akt Signaling Pathway by Activating Grb2.14 inhibitors1.5 x 10^6 cells2 Pieces/Box7 inhibitors2 Pieces/Box1 mg2 Pieces/Box11 inhibitors2 Pieces/Box2 Pieces/Box1.5x10(6) cells2 Pieces/Box
#33585557 2021/01/29 To Up
Long Non-coding RNA BTG3-7:1 and JUND Co-regulate to Promote Triple-Negative Breast Cancer Progress.Triple-negative breast cancer (TNBC) is a type of highly invasive breast cancer with poor prognosis. Recently, massive data reveal that long non-coding RNAs (lncRNAs) play important roles in cancer progress. Recently, although the role of lncRNAs in breast cancer has been well documented, few focused on TNBC. In this study, we aimed to systematically identify functional lncRNAs and to explore its molecular mechanism on TNBC progress.
Zheng Dan, He Xiujing, Luo Ting, Zhong Xiaorong, Zheng Hong, Yang Jiqiao, Li Yanchu, Jing Jing
2371 related Products with: Long Non-coding RNA BTG3-7:1 and JUND Co-regulate to Promote Triple-Negative Breast Cancer Progress.100ul100ul100ul100ul100ul 100ul100ul1000
#33584322 2021/02/02 To Up
Enhanced Autophagy in GAB1-Deficient Vascular Endothelial Cells Is Responsible for Atherosclerosis Progression.Autophagy is a host machinery that controls cellular health. Dysfunction of autophagy is responsible for the pathogenesis of many human diseases that include atherosclerosis obliterans (ASO). Physiologically, host autophagy removes aging organelles and delays the formation of atherosclerotic plaque. However, in ischemia event, dysregulated autophagy can be induced to trigger autosis, leading to an inevitable cellular death. Grb2-associated binder 1 (GAB1) is a docking/scaffolding adaptor protein that regulates many cell processes including autophagy. Our study first reported that the protein expression of GAB1 significantly decreased in ASO. Mechanically, our results showed that inhibition of Akt (protein kinase B), the upstream of mTOR (mechanistic target of rapamycin), significantly enhanced autophagy by demonstrating the downregulation of p62/Sequestosome 1 expression and the upregulation of the ratio of LC3II/LC3I. Conversely, we found that the inhibition of ERK1/2 (extracellular signal-regulated kinases1/2), p38, and JNK (c-Jun N-terminal kinase) signaling pathway, respectively, significantly inhibited autophagy by demonstrating the upregulation of p62 expression and the downregulation of the ratio of LC3II/LC3I. Further, we demonstrated that knockdown of GAB1 significantly increased autophagy in HUVECs (human umbilical vein endothelial cells) activation of MAPK (mitogen-activated protein kinase) pathways that include ERK1/2, p38, and JNK. Moreover, we found that knockdown of GAB1 profoundly inhibited HUVEC proliferation, migration, and tube formation. Taken together, this study first suggests that GAB1 is a key regulator of autophagy in HUVECs. Targeting GAB1 may serve as a potential strategy for the atherosclerosis treatment.
Xin Qian, Han Wang, Yuli Wang, Jiaquan Chen, Xiangjiang Guo, Haoyu Deng
2378 related Products with: Enhanced Autophagy in GAB1-Deficient Vascular Endothelial Cells Is Responsible for Atherosclerosis Progression.1.00 flask1.00 flask1.00 flask1.00 flask100 μg1.00 flask100ug Lyophilized100ug Lyophilized 1 G1 Set100ug Lyophilized
#33555447 2021/02/08 To Up
Medulloblastoma: clinicopathological parameters, risk stratification, and survival analysis of immunohistochemically validated molecular subgroups.Medulloblastoma (MB) is a heterogeneous disease, displaying distinct genetic profiles with specific molecular subgroups. This study aimed to validate MB molecular subgrouping using surrogate immunohistochemistry and associate molecular subgroups, histopathological types, and available clinicopathological parameters with overall survival (OS) and progression-free survival (PFS) of MB patients. This study included 40 MBs; immunohistochemical staining, using β-catenin and GRB2-Associated Binding Protein 1 (GAB1) antibodies, was used to classify MB cases into wingless signaling activated (WNT), sonic hedgehog (SHH), and non-WNT/SHH molecular subgroups. Nuclear morphometric analysis (for assessment of degree of anaplasia) and Kaplan-Meier survival curves were done.
Asmaa Mustafa Eid, Nehal Abd El-Ghaffar Heabah
1369 related Products with: Medulloblastoma: clinicopathological parameters, risk stratification, and survival analysis of immunohistochemically validated molecular subgroups.6 ml Ready-to-use 1 module1 module 25 MG1 g100ul1 module1 g25 mg1 module
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