Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Keizer1996_Ryanodine_receptor_adaptation

ABSTRACT: The model reproduces the time profile of Open probability of the ryanodine receptor as shown in Fig 2A and 2B of the paper. The model was successfully tested on MathSBML and Jarnac. To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information. In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not. To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.

SUBMITTER: Harish Dharuri

PROVIDER: BIOMD0000000060 | BioModels | 2008-10-01

REPOSITORIES: BioModels

ACCESS DATA

Json Xml

Publications

Ryanodine receptor adaptation and Ca2+(-)induced Ca2+ release-dependent Ca2+ oscillations.

Keizer J J Levine L L

Biophysical journal 19961201 6

A simplified mechanism that mimics "adaptation" of the ryanodine receptor (RyR) has been developed and its significance for Ca2+(-)induced Ca2+ release and Ca2+ oscillations investigated. For parameters that reproduce experimental data for the RyR from cardiac cells, adaptation of the RyR in combination with sarco/endoplasmic reticulum Ca2+ ATPase Ca2+ pumps in the internal stores can give rise to either low [Cai2+] steady states or Ca2+ oscillations coexisting with unphysiologically high [Cai2+ ...[more]

PMID: 8968617

Similar Datasets

Glucagon receptor signaling in GCGR KO mice

Project description:GCGR wt and ko mice Glucagon receptor signaling in GCGR KO mice: fig 2a in Solloway et al.

2015-06-02 | GSE68143 | GEO

Human cerebrospinal fluid autoantibody lipid microarray profiling

Project description:This SuperSeries is composed of the following subset Series: GSE37664: Human cerebrospinal fluid autoantibody lipid microarray profiling (Fig. 1A) GSE37670: Human cerebrospinal fluid autoantibody lipid microarray profiling (Fig. 2A) GSE37826: Human cerebrospinal fluid autoantibody lipid microarray profiling (Fig. 2C) Refer to individual Series

2012-05-08 | E-GEOD-37830 | biostudies-arrayexpress

The FAK-Inhibitor BI 853520 exerts anti-tumor effects in breast cancer

Project description:In order to delineate the molecular mechanisms leading to the therapeutic effect of BI 853520 on primary tumor growth, mice harboring 4T1 primary tumors were treated for five days with BI 853520, and RNA extracted from total tumors was subjected to next generation sequencing. Only primary tumors with sufficient RNA quality were included into further analysis (Suppl. Fig. 2A). Gene expression correlation analysis displayed a clear separation of transcriptomic profiles derived from primary tumors of mice treated with BI 853520 or vehicle (Suppl. Fig. 2B). Comparative gene expression analysis of primary tumors of mice treated with BI 853520 versus vehicle control revealed 1293 upregulated and 475 downregulated genes (cutoffs: p-value ≤ 0.05, fold change +/- 1.5). Functional enrichment analysis for biological processes and signaling pathways indicated that the regulation of epithelial cell proliferation, positive regulation of cell cycle/cell proliferation/cell division and regulation of cell proliferation/cell division/cell growth were enriched in genes downregulated by BI 853520 treatment (Fig. 3A). In line with this finding, gene set enrichment analysis confirmed a significant reduction in the relative expression of genes important for cell cycle and positive regulation of mitotic cell cycle (including cyclin-dependent kinase 1 and 4; Cdk1: log2 fold-change= -0.4519, FDR= 4.24e-03; Cdk4: log2 fold-change= -0.3072, FDR= 0.003718), while the negative regulation of cell proliferation was increased following BI 853520 treatment (Fig. 3C; Suppl. Fig. 2C).

2019-07-19 | GSE116117 | GEO

ADAM9 Up-regulates N-Cadherin via MiR-218 Suppression in Lung Adenocarcinoma Cells

Project description:Identification of miRNAs that differentially expressed in brain metastatic cells and were predicted to target CDH2. To investigate which miRNAs could regulate CDH2 expression in brain-metastatic lung cancer cells, we examined the miRNA expression profiles in brain-metastatic lung cancer cells and their parental cells using Illumina miRNA microarray. By comparing the endogenous expression of all miRNAs, 146 miRNAs were selected by 2-fold changes in brain-metastatic lung cancer cells. Furthermore, we used several algorithms in miRSystem to predict which miRNA whose target gene was CDH2. There were 44 miRNAs that were predicted to target CDH2. In total, we identified nine miRNAs whose target gene was CDH2 and whose expression was significantly different between the highly metastatic cells and their parental cells (Fig. 2A). Among these miRNAs, four miRNAs were found to be down-regulated and five miRNAs were up-regulated in brain-metastatic lung cancer cells (Fig. 2B).

2016-10-11 | GSE51666 | GEO

Treatment of extracellular vesicles change gene expression in mesothelial cells

Project description:To investigate whether the EVs from cancer cell lines could change gene expression in mesothelial cells, the EVs from five types of cells (ES-2 cells, A2780 cells, SKOV3 cells, HOSE1 cells and HOSE2 cells) were added to MeT-5A cells (Fig. 2a). All three selected cancer cell lines expressed metastatic phenotypes in mouse model (Fig. 1c), and EVs from HOSE2 cell line, established together with HOSE1 cell line, was also set as control. Total mRNAs were extracted by MeT-5A cells treated with EVs, and then microarray analysis was performed.

2017-06-12 | GSE80125 | GEO

Sneyd2002_IP3_Receptor

Project description:This model was successfully tested on Jarnac and MathSBML. The model reproduces the time profile of "Open Probability" of the receptor as shown in Figure 4 of the publication. The value of calcium ion concentration "c" in this model is 10 microM. To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information. In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not. To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.

2006-05-30 | BIOMD0000000057 | BioModels

NKTR-102 in Combination With Cetuximab in Patients With Refractory Solid Tumors (Phase 2a) and Metastatic or Locally Advanced Colorectal Cancer (Phase 2b)

Project description:Study 07-PIR-02 is a Phase 2 study designed to evaluate the safety and efficacy of NKTR-102 (PEG-irinotecan) for the treatment of patients with colorectal cancer (CRC). The study is comprised of two sequential components - Phase 2a and Phase 2b. The Phase 2a portion is an open-label, dose-finding trial in multiple solid tumor types that are refractory to standard curative or palliative therapies. The primary endpoint of the Phase 2a is to establish the /recommended Phase 2 Dose (RPTD) of NKTR-102 by measuring the frequency of Dose Limiting Toxicity (DLT). The Phase 2b portion is an open-label, randomized, two-arm study in patients with second-line metastatic colorectal cancer and study participants will be randomized (1:1) to receive either NKTR-102 and cetuximab or irinotecan and cetuximab. The primary endpoint of the Phase 2b portion of the trial is progression-free survival. Secondary endpoints for both the Phase 2a and 2b portion include response rate, response duration, overall survival, standard pharmacokinetics, and incidence of toxicities, including diarrhea and neutropenia.

| 2049422 | ecrin-mdr-crc

Anti-GCGR antibody treatment in db/db mice

Project description:Gene expression of liver tissue from db/db untreated (6x replicates) and db/db treated with 5mg/kg of 3c7.v44 mAb (6x replicates). Anti-GCGR antibody treatment in db/db mice: fig 2b in Solloway et al.

2015-06-02 | GSE68142 | GEO

Weimann2004_CircadianOscillator

Project description:The model reproduces the time profile of the species as depicted in Fig 3A of the paper. Model successfully tested on MathSBML and Jarnac.

2008-04-16 | BIOMD0000000170 | BioModels

Role of AP-2a/AP-2b transcription factors in the adult epidermis.

Project description:To investigate the effects of inactivation of the transcription factors AP-2a and/or AP-2b in the adult mouse skin.

2023-12-20 | GSE248372 | GEO