Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ABSTRACT: a small-molecule kinase inhibitor

PROVIDER: PRJNA602151 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR10914765_1.fastq.gz	Fastqsanger.gz
	SRR10914765_2.fastq.gz	Fastqsanger.gz
	SRR10914766_1.fastq.gz	Fastqsanger.gz
	SRR10914766_2.fastq.gz	Fastqsanger.gz
	SRR10914767_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Project description:A small molecule ATM kinase inhibitor increases CRISPR/Cas9 1-bp insertion frequency

| PRJNA658607 | ENA

RNA-seq of cancer cell lines treated with T-025

Project description:4 cancer cell lines were treated with T-025 for 6 hours T-025 is a novel small molecule inhibitor of CLK. CLK is a kinase that regulates pre-mRNA splicing.

2018-05-01 | GSE101540 | GEO

Chronologically Modified Androgen Receptor in Recurrent Castration Resistant Prostate Cancer and its therapeutic targeting

Project description:We uncovered a novel acetylation event at Lys609 in the Zinc finger DNA binding domain of AR (acK609-AR) that altered global transcription program, bestowing insensitivity for enzalutamide and abiraterone. ACK1 kinase small molecule inhibitor, (R)-9b not only curbed K609-acetylation, but also significantly compromised enzalutamide-resistant CRPC tumor growth.

2021-06-01 | GSE162761 | GEO

Evaluation of Trastuzumab in Combination With Lapatinib or Pertuzumab in Combination With Trastuzumab-Emtansine to Treat Patients With HER2-positive Metastatic Colorectal Cancer

Project description:This is a Phase II multi-center 2-sequential cohorts trial, designed to assess the objective response rate of two anti HER2 combination in advanced disease CRC patients harbouring an amplified HER2 tumor assessed according to HERACLES Diagnostic Criteria by FISH/SISH. Cohort A: monoclonal antibody trastuzumab, used in combination with the small molecule tyrosine kinase inhibitor lapatinib. Cohort B, monoclonal antibody pertuzumab, used in combination with the antibody drug conjugate trastuzumab-emtansine. Please note that cohort A accrual has been closed and endpoint already reached.

| 2249965 | ecrin-mdr-crc

Transcription profiling of mouse CD8-IGF1R 3T3 cells and 3T3 Vector control treated for 24 h with vehicle or IGF1R inhibitor A-928605 reveals reversal of oncogene transformation and suppression of tumor growth by the novel IGF1R kinase inhibitor A-928605.

Project description:The insulin-like growth factor (IGF) axis is an important signaling pathway in the growth and survival of many cell types and has been implicated in multiple aspects of cancer progression from tumorigenesis to metastasis. The multiple roles of IGF signaling in cancer suggest that selective inhibition of the pathway might yield clinically effective therapeutics. Here we describe A-928605, a novel small molecule inhibitor of the receptor tyrosine kinase responsible for IGF signal transduction. This small molecule is able to abrogate activation of the pathway as shown by effects on the target and downstream effectors and is shown to be effective at inhibiting the proliferation of an oncogene addicted tumor model cell line (CD8-IGF1R 3T3) both in vitro and in vivo. Experiment Overall Design: CD8-IGF1R 3T3 cells and 3T3 Vector control treated for 24 h with vehicle or IGF1R inhibitor A-928605, all with 3 replicates.

2009-06-11 | E-GEOD-14024 | biostudies-arrayexpress

Stimulation of fracture mineralization by salt-inducible kinase inhibitors

Project description:Over 6.8 million fractures are reported annually in the US, accounting for 20% of all musculoskeletal injuries. Approximately 10% of fractures will experience delayed- or non-union. Parathyroid hormone (PTH) analogs and anabolic osteoporosis therapeutics can stimulate fracture repair in animal models and patients with chronic nonunion. Previous studies have demonstrated that small molecule salt inducible kinase (SIK) inhibitors mimic PTH action in vitro and in vivo. Therefore, we hypothesize that YKL-05-099, a small molecule SIK inhibitor, will accelerate fracture callus osteogenesis.

2024-09-01 | GSE266115 | GEO

Compensatory IKKa activation of classical NF-kB signaling during IKKb inhibition

Project description:A subtype of diffuse large B-cell lymphoma (DLBCL), termed activated B-cell-like (ABC) DLBCL, depends on constitutive NF-kB pathway signaling for survival. Small molecule inhibitors of IkB kinase b (IKKb), a key regulator of the NF-kB pathway, kill ABC DLBCL cells and hold promise for the treatment of this lymphoma type. We conducted an RNA interference genetic screen to investigate potential mechanisms of resistance of ABC DLBCL cells to IKKb inhibitors. We screened a library of small hairpin RNAs (shRNAs) targeting 500 protein kinases for shRNAs that would kill an ABC DLBCL cell line in the presence of a small molecule IKKb inhibitor more effectively than in its absence. Two independent shRNAs targeting IKKa synergized with the IKKb inhibitor to kill three different ABC DLBCL cell lines but were not toxic by themselves. Surprisingly, IKKa shRNAs blocked the classical rather than the alternative NF-kB pathway in ABC DLBCL cells, as judged by inhibition of IkBa phosphorylation. IKKa shRNA toxicity was reversed by coexpression of wild type but not kinase inactive forms of IKKa, suggesting that IKKa may directly phosphorylate IkBa under conditions of IKKb inhibition. These results suggest that therapy for ABC DLBCL may be improved by targeting both IKKa and IKKb. Keywords: compound treatment design Gene expression profiling of OCI-Ly3 cells with or without expressing IKKa shRNA in the presence or absence of 12.5 uM IKKb inhibitor for 2 and 3 days. Four samples were analyzed.

2009-06-01 | E-GEOD-11902 | biostudies-arrayexpress

Genome-wide analysis of time-dependent gene expression in SUM-225 cells treated with the HER-2-specific inhibitor CP724,714 for 45 hours

Project description:Results of blocking the HER-2 oncogene kinase function in SUM-225 cells by treatment with CP724,714 and measuring gene expression as a function of time provides information as to what genes are regulated by HER-2 in this breast cancer cell line. SUM-225 cells were treated with the HER-2-specific small molecule kinase inhibitor CP724,714 for 45 hours. Total RNA was collected every 3 hours from parallel cultures throughout the 45 hour duration of treatment and genome-wide analysis of expression was performed on RNA from each time point (total 16 time points, starting at 0 hours treatment).

2011-03-18 | E-GEOD-22955 | biostudies-arrayexpress

Genome-wide analysis of time-dependent gene expression in MCF-10A cells treated with the EGFR-specific inhibitor gefitinib for 45 hours

Project description:Results of blocking EGFR kinase activity in MCF-10A cells by treatment with gefitinib and measuring gene expression as a function of time provides information as to what genes are regulated by EGFR in these nontransformed breast epithelial cells. MCF-10A cells were treated with the EGFR-specific small molecule kinase inhibitor gefitinib for 45 hours. Total RNA was collected every 3 hours from parallel cultures throughout the 45 hour duration of treatment and genome-wide analysis of expression was performed on RNA from each time point (total 16 time points, starting at 0 hours treatment).

2010-08-24 | E-GEOD-23135 | biostudies-arrayexpress

Genome-wide analysis of time-dependent gene expression in MCF-10A cells treated with the HER-2-specific inhibitor CP724,714 for 45 hours

Project description:Results of blocking HER-2 kinase activity in MCF-10A cells by treatment with CP724,714 and measuring gene expression as a function of time provides information as to what genes are regulated by HER-2 in these nontransformed breast epithelial cells. MCF-10A cells were treated with the HER-2-specific small molecule kinase inhibitor CP724,714 for 45 hours. Total RNA was collected every 3 hours from parallel cultures throughout the 45 hour duration of treatment and genome-wide analysis of expression was performed on RNA from each time point (total 16 time points, starting at 0 hours treatment).

2011-03-18 | E-GEOD-23138 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data