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ITRAQ analysis of K562 cell line

ABSTRACT: K562 cells untreated (S) and treated (S+IM) with Imatinib as well as sensitive (S+IM) and resistant (R) to imatinib were subjected to labelled quantification by iTRAQ to identify Bcr-Abl downstream signaling components and proteins modulated in resistance respectively

INSTRUMENT(S): TripleTOF 5600

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Suspension Culture

SUBMITTER: Mythreyi Narasimhan

LAB HEAD: Dr. Rukmini Govekar

PROVIDER: PXD025173 | Pride | 2021-10-05

REPOSITORIES: Pride

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			Action	DRS
	K562_S_IM_vs_R-100mM_run_2.wiff	Wiff
	K562_S_IM_vs_R-100mM_run_2.wiff.scan	Wiff
	K562_S_IM_vs_R-150mM_run_2.wiff	Wiff
	K562_S_IM_vs_R-150mM_run_2.wiff.scan	Wiff
	K562_S_IM_vs_R-200mM_run_2.wiff	Wiff

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1 - 5 of 59

Publications

Atypical activation of signaling downstream of inactivated Bcr-Abl mediates chemoresistance in chronic myeloid leukemia.

Narasimhan Mythreyi M Khamkar Vaishnavi V Tilwani Sarika S Dalal Sorab N SN Shetty Dhanlaxmi D Subramanian P G PG Gupta Sanjay S Govekar Rukmini R

Journal of cell communication and signaling 20211001 2

Chronic myeloid leukemia (CML) epitomises successful targeted therapy, where inhibition of tyrosine kinase activity of oncoprotein Bcr-Abl1 by imatinib, induces remission in 86% patients in initial chronic phase (CP). However, in acute phase of blast crisis, 80% patients show resistance, 40% among them despite inhibition of Bcr-Abl1 activity. This implies activation of either Bcr-Abl1- independent signalling pathways or restoration of signalling downstream of inactive Bcr-Abl1. In the present st ...[more]

PMID: 34596797

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Identify Novel Iron–Transporting Proteins in Streptococcus pneumoniae

Project description:Streptococcus pneumoniae (S. pneumoniae) is a major human pathogen causing morbidity and mortality worldwide. Efficiently acquiring iron from the environment is critical for S. pneumoniae to sustain growth and cause infection. There are only three known iron-uptake systems in Streptococcal species responsible for iron acquisition from the host, including ABC transporters PiaABC, PiuABC and PitABC. Besides, no other iron-transporting system has been suggested. In this work, we employed our newly established translating mRNA analysis integrated with proteomics to evaluate the possible existence of novel iron transporters in the bacterium. We simultaneously deleted the iron-binding protein genes of the three iron-uptake systems to construct a piaA/piuA/pitA triple mutant (Tri-Mut) of S. pneumoniae D39, in which genes and proteins related to iron transport should be regulated in response to the deletion. With ribosome associated mRNA sequencing-based translatomics focusing on translating mRNA and iTRAQ quantitative proteomics based on the covalent labeling of peptides with tags of varying mass, we indeed observed a large number of genes and proteins representing various coordinated biological pathways with significantly altered expression levels in the Tri-Mut mutant. Highlighted in this observation is the identification of several new potential iron-uptake ABC transporters for Streptococcal iron metabolism. In particular, putative protein SPD_1609 in operon 804 was verified to be a novel iron-binding protein with similar function to PitA in S. pneumoniae. These data derived from the integrative translatomics and proteomics analyses provided rich information and insightful clues for further investigations on iron-transporting mechanism in bacteria and the interplay between Streptococcal iron availability and the biological metabolic pathways.

2018-10-26 | PXD003313 | Pride

Gene expression profile induced by Imatinib

Project description:Activation-induced cytidine deaminase (AID) is essential for class switch recombination (CSR) and somatic hypermutation (SHM). Its deregulated expression acts as a genomic mutator that can contribute to the development of various malignancies. During treatment with imatinib mesylate (IM), patients with chronic myeloid leukemia (CML) often develop hypogammaglobulinemia, the mechanism of which has not yet been clarified. Here, we provide evidence that CSR upon B cell activation is apparently inhibited by IM through downregulation of AID. Furthermore, expression of E2A, a key transcription factor for AID induction, was markedly suppressed by IM. These results elucidate not only the underlying mechanism of IM-induced hypogammaglobulinemia but also its potential efficacy as an AID suppressor. We investigated that class switch recombination(CSR) upon B cell activation is apparently inhibited by imatinib mesylate(IM) through downregulation of activation-induced cytidine deaminase(AID). Furthermore, expression of E2A was markedly suppressed by IM. To elucidate the more detailed pathway, we performed the microarray analysis. Microarray analysis was performed on splenocytes cultured for 72 h in the presence or absence of 10 µM Imatinib. The mouse splenocytes were cultured for 72 h with or without 10 µM Imatinib (IM) in conditioning medium containing IL-4 and LPS. RNA from 1X10^6 splenocytes used for microarray analysis was isolated using the RNeasy Mini Kit (50) (Qiagen, Hilden, Germany).　Gene expression microarray analysis was performed using one-color microarray-based gene-expression analysis (Agilent Technologies, Santa Clara, CA, USA) according to the manufacturer’s instructions. After scanning, expression values for the genes were determined using GeneSpringGX software.

2012-02-08 | E-GEOD-35559 | biostudies-arrayexpress

Transcription profiling of human gastrointestinal stromal tumour is predictive of rapid response to imatinib mesylate

Project description:Gene expression profiling using oligonucleotide microarrays performed on tumor samples obtained before and after imatinib mesylate (IM) therapy. Rapid responding (to IM) samples were compared to non-responding/stable disease samples as measured by CT scan measurements to identify a gene signature that can predict rapid response to IM. Experiment Overall Design: 54 samples, 29 pre-treatment biopsy samples, 25 post-treatment/post-surgery tumor samples from Gastrointestinal Stromal Tumors

2009-12-02 | E-GEOD-15966 | biostudies-arrayexpress

Molecular comparison of imatinib-naïve and resistant gastrointestinal stromal tumors: differentially expressed microRNAs and mRNAs

Project description:Despite the success of imatinib in advanced gastrointestinal stromal tumor (GIST) patients, 50% of the patients experience resistance within two years of treatment underscoring the need to get better insight into the mechanisms conferring imatinib resistance. Here the microRNA and mRNA expression profiles in primary (imatinib-naïve) and imatinib-resistant GIST were examined. Fifty-three GIST samples harboring primary KIT mutations (exon 9; n=11/exon 11; n=41/exon 17; n=1) and comprising imatinib-naïve (IM-n) (n=33) and imatinib-resistant (IM-r) (n=20) tumors, were analyzed. The microRNA expression profiles were determined and from a subset (IM-n, n=14; IM-r, n=15) the mRNA expression profile was established. Ingenuity pathway analyses were used to unravel biochemical pathways and gene networks in IM-r GIST. Thirty-five differentially expressed miRNAs between IM-n and IM-r GIST samples were identified. Additionally, miRNAs distinguished IM-r samples with and without secondary KIT mutations. Furthermore 352 aberrantly expressed genes were found in IM-r samples. Pathway and network analyses revealed an association of differentially expressed genes with cell cycle progression and cellular proliferation thereby implicating genes and pathways involved in imatinib resistance in GIST. Differentially expressed miRNAs and mRNAs between IM-n and IM-r GIST were identified. Bioinformatic analyses provided insight into the genes and biochemical pathways involved in imatinib-resistance and highlighted key genes that may be putative treatment targets.

2019-06-12 | GSE132542 | GEO

Expression profiling in extracellular miRNAs (plasma miRNAs) of CML patients after imatinib discontinuation (STOP-IM)

Project description:An approximately 40% of chronic myeloid leukemia (CML) patients who discontinued imatinib (IM) therapy maintained undetectable minimal residual disease (UMRD) for more than one year (STOP-IM). We set out to examine plasma miRNAs expression in CML patients who could discontinue IM, to seek the possible distinguishable biomarker in STOP-IM CML patients. We compared CML patients who sustained UMRD for more than one year after discontinuation of imatinib (STOP-IM group) with healthy volunteers (controls). In 7 patients who had discontinued IM with sustained UMRD for more than 6 months (STOP-IM group), samples were collected when IM was stopped. Seven healthy volunteers served as control. Plasma samples were harvested form 2ml of whole blood. Isolation of total RNA was performed using the mirVana PARIS kit (Ambion, Austin, TX, USA). The expression profile of miRNAs was determined using the Human Taqman miRNA Arrays A (Applied Biosystems). Synthetic ath-miR-159 (Hokkaido System Science, Hokkaido, Japan) were used as a control. QRT-PCR was carried out on an Applied Biosystems 7900HT thermal cycler using the manufacturerâ??s recommended program. With the use of SDS2.2 software and Data Assist (Thermo Fisher Sciences), the expression of plasma miRNAs was calculated based on cycle threshold (Ct) values normalized by those of ath-miR-159, which was spiked in each plasma sample. Data analysis was done using GeneSiferâ?? software (Perkin Elmer, Waltham, MA, USA). The Benjamini-Hochberg algorithm was used for estimation of false discovery rates.

2016-03-31 | E-GEOD-75391 | biostudies-arrayexpress

LC-MSMS of leukemic cell line K562

Project description:Comparative label free quantitative proteomic analysis using SWATH-MS has been carried out for K562 cells treated with Imatinib (S+IM) against untreated K562 (S) as well as imatinib resistant K562 cells (R). Compariosn of S+IM vs R constitutes Dataset 1 while that of S vs S+IM constitutes dataset 2

2019-06-14 | PXD009686 | Pride

Expression profiling in extracellular miRNAs (plasma miRNAs) of CML patients after imatinib discontinuation (STOP-IM)

2016-03-31 | GSE75391 | GEO

Expression profiling in extracellular miRNAs (exosomal miRNAs) of CML patients after imatinib discontinuation (STOP-IM)

2016-03-31 | GSE75389 | GEO

Quantitative proteomic analysis of plasma exosomes to identify the candidate biomarker of Imatinib Resistance in Chronic Myeloid Leukemia patients

Project description:Imatinib (IM), a tyrosine kinase inhibitor (TKI), has markedly improved the survival and life quality of chronic myeloid leukemia (CML) patients. However, the lack of speciﬁc biomarkers for IM resistance remains a serious clinical challenge. Recently, growing evidence has suggested that exosome-harbored proteins were involved in tumor drug resistance and could be novel biomarkers for the diagnosis and drug sensitivity prediction of cancer. Therefore, we aimed to investigate the proteomic proﬁle of plasma exosomes derived from CML patients to identify ideal biomarkers for IM resistance. We extracted exosomes from pooled plasma samples of 9 imatinib-resistant CML patients and 9 imatinib-sensitive CML patients by ultracentrifugation. Then, we identified the expression levels of exosomal proteins by liquid chromatography-tandem mass spectrometry (LC-MS/MS) based label free quantification. Bioinformatics analyses were used to analyze the proteomic data. we found that RPL13 and RPL14 exhibited exceptional upregulation in imatinib-resistant CML patients, which were further confirmed by PRM and WB. Proteomic analysis of plasma exosomes provides new ideas and important information for the study of IM resistance in CML. Especially the exosomal proteins (RPL13 and RPL14), which may have great potential as biomarkers of IM resistance.

2022-02-16 | PXD028779 | Pride

Wdr13-/0 compared to wild-type mice hippocampus and pre-frontal cortex iTRAQ proteomics

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2017-01-03 | PXD002466 | Pride

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