TOB1 Blocking Peptide, Blocking Peptides
- Known as:
- TOB1 Blocking Peptide, Blocking Peptides
- Catalog number:
- 33R-7679
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Fitzgerald
- Gene target:
- TOB1 Blocking Peptide Peptides
Related genes to: TOB1 Blocking Peptide, Blocking Peptides
- Gene:
- TOB1 NIH gene
- Name:
- transducer of ERBB2, 1
- Previous symbol:
- TROB1
- Synonyms:
- TOB, TROB, APRO5
- Chromosome:
- 17q21.33
- Locus Type:
- gene with protein product
- Date approved:
- 2000-06-01
- Date modifiied:
- 2016-07-04
Related products to: TOB1 Blocking Peptide, Blocking Peptides
Related articles to: TOB1 Blocking Peptide, Blocking Peptides
- To be clinically useful in goal-directed fluid therapy, a fluid challenge (FC) must achieve a large enough blood volume change (ΔBV) to materially change ventricular preload and stroke volume (ΔSV). The same % change in BV for all the subsequent FCs must also be achieved. We explored under what circumstances these prerequisites can be met by referring to data from a clinical trial where 111 patients underwent three successive intravenous FCs using crystalloid (Ringer´s lactate) or colloid (hydroxyethyl starch), involving a total of 9 mL/kg of fluid, just after induction of general anaesthesia. - Source: PubMed
Publication date: 2026/05/22
O'Brien TerryHahn Robert G - Thymoquinone (TQ), the principal bioactive component of Nigella sativa, has attracted considerable attention for its potential anticancer properties. However, its antiproliferative effects and the underlying molecular mechanisms across different cancer cell types remain incompletely understood. - Source: PubMed
Publication date: 2026/05/22
Yüce HandeBerberoğlu YaseminAşkın Özek DilanÜnüvar Songül - Elevated sodium concentrations are commonly observed in tumors and sites of inflammation. Previous studies have shown that high salt levels modulate the phenotype and function of CD4 and CD8 T cells, regulatory T cells, and macrophages. In this study, we performed transcriptomic studies that revealed profound alterations in the neutrophil transcriptome upon high salt exposure, with changes that significantly exceeded those triggered by conventional agonists. By integrating transcriptomic data with functional assays, our findings suggest that high salt-induced neutrophil activation involves mitochondrial ROS production, which subsequently activates p38 MAPK and engages FOS-, Bruton's tyrosine kinase (BTK)-, and cyclooxygenase 2 (COX2)-dependent pathways. Remarkably, the plasticity of the neutrophil transcriptome in response to high salt was further evidenced by the upregulation of genes typically associated with other cell types, including semenogelin 1 (), intercellular adhesion molecule-4 (), tripartite motif69 (), amphiregulin (), oncostatin (), and transducer of ERBB2-1 (), suggesting a broader role for neutrophils in different biological processes beyond their participation in innate immunity. - Source: PubMed
Publication date: 2026/01/21
Mazzitelli IgnacioBleichmar LucíaRivelli FedericoFeijoo IngridAdamczyk AlanCabrerizo GonzaloErra Díaz FernandoGeffner Jorge - Due to the growing number of Alzheimer's disease (AD) patients, new drugs are urgently required. A synthetic nonapeptide, JAL-TA9 (YKGSGFRMI), derived from Transducer of ErbB-2.1 (Tob1) protein, cleaves amyloid β (Aβ) 42 with serine protease-like activity. Aβ25-35 was chosen because it is the shortest fragment that forms fibrils and is cytotoxic. Aβ25-35 has been used to create AD model mice, and it appears to be an attractive target for AD therapeutics. Using Thioflavin-T assays, the fluorescence intensity of the reaction of Aβ25-35 and JAL-TA9 was lower than that of Aβ25-35 without JAL-TA9, and the same result was obtained with aggregated Aβ25-35. These data showed that JAL-TA9 inhibits aggregation of Aβ25-35 and dissolves its aggregates. Furthermore, electron microscopy showed that amyloid fibrils of both Aβ25-35 and aggregated Aβ25-35 are reduced in the presence of JAL-TA9. The proteolytic activity of JAL-TA9 against Aβ25-35 was evaluated using HPLC and mass spectrometry. These data showed that JAL-TA9 cleaves both soluble and aggregated forms of Aβ25-35. JAL-TA9 inhibits neuronal cytotoxicity caused by Aβ25-35 aggregation by cleaving Aβ25-35 and its aggregated form. These results suggest that JAL-TA9 is a promising candidate for developing novel drugs against AD. - Source: PubMed
Publication date: 2025/09/03
Nakamura RinaOkada MomokaTakahashi AsukaHayashi YoshihiroKonishi MotomiIto FumiakiMurakami IchiroSaito MotoakiAkizawa Toshifumi - Endoplasmic reticulum stress and glucose supply are significant factors in glioblastoma growth. The present study aims to investigate the impact of glucose-dependent control of , , , , , and gene expression in U87MG glioblastoma cells in response to the inhibition of both enzymatic activities of signaling protein ERN1. The U87MG glioblastoma cells with inhibited both enzymatic activities of ERN1 (endoribonuclease and protein kinase; dnERN1) were used. Cells transfected with an empty vector served as a control. The expression level of the and other genes was studied by quantitative RT-PCR. It was shown that the expression level of the gene is up-regulated, while that of and genes is down-regulated in control glioblastoma cells treated with glucose deprivation. Nevertheless, the ERN1 knockdown modified the sensitivity of and genes to reduced glucose supply. At the same time, the expression of , , and genes in control glioblastoma cells was resistant to glucose deprivation conditions. However, inhibition of the enzymatic activities of ERN1 signaling protein strongly increased the impact of glucose deprivation on gene expression, but down-regulated the expression of the gene. These results demonstrate that the enzymatic activity of signaling protein ERN1 controls the sensitivity of almost all studied genes to glucose deprivation in U87MG glioblastoma cells in a gene-specific manner. This is important for elucidating the endoplasmic reticulum stress-mediated sensitivity of key regulatory gene expression in glioblastoma cells to glucose supply, a significant factor in tumor growth. - Source: PubMed
Publication date: 2025/08/28
Minchenko Oleksandr HViletska Yuliia MSliusar Myroslava YHnatiuk Oksana SRatushna Oksana OFeldman Taia VKozynkevych Halyna EBezrodnyi Borys HMinchenko Dmytro O