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Article ; Online: Detection of driver mutations in plasma cell-free nucleic acids in differentiated thyroid neoplasm.

Dutta, Susmita / Tarafdar, Soham / Mukhopadhyay, Pradip / Bhattacharyya, Nitai P / Ghosh, Sujoy

2023 Volume 188, Issue 1

Abstract: Importance: This proof-of-concept paper demonstrates that driver mutations can be detected in plasma in differentiated thyroid tumors, and we were able to detect mutations in upto 80% malignant thyroid nodules. Additionally, cancer subtypes could also ... ...

Abstract	Importance: This proof-of-concept paper demonstrates that driver mutations can be detected in plasma in differentiated thyroid tumors, and we were able to detect mutations in upto 80% malignant thyroid nodules. Additionally, cancer subtypes could also be predicted using a 8-gene panel. In almost 90% follicular adenoma, rat sarcoma virus (RAS) mutations were detectable. There was a strong agreement between driver mutations found in plasma samples, FNAC materials, and histopathology samples. This has potential as a noninvasive, preoperative diagnostic tool (particularly of clinical importance in indeterminate nodules) and may help in detection of residual tumor after surgery. Future research is warranted to test the role of this tool to detect tumor recurrence. Objective: Ultrasonographic (USG) evaluation and fine-needle aspiration (FNA) are cornerstone for evaluation of thyroid neoplasm. Molecular technique including detection of driver mutation from FNA cytology (FNAC) material is an established modality. In this study, we explored the feasibility of using plasma cell-free nucleic acids to identify known driver mutations in differentiated thyroid neoplasm. Design: Patients presenting with thyroid nodules underwent USG with Thyroid Image Reporting and Data Systems scoring and FNAC (Bethesda classification). All patients in Bethesda 3, 4, 5, 6 underwent surgery and histopathological confirmation. Patients in Bethesda 2 (cosmetic concerns, compressive symptoms) underwent surgery, and rest were presumed benign on the basis of USG, FNAC features, and clinical followup.). Setting: Endocrinology clinic. Participants: Subjects with thyroid nodule. Intervention(s) or exposure(s): None. Main outcome(s) and measure(s): Plasma sample, FNA, and histopathology material were evaluated for driver mutations (8-gene panel comprising BRAF-V600E, RET/PTC3, RET/PTC1, TERT promoter, HRAS, NRAS, KRAS, and PAX8-PPARG). Results: A total of 223 subjects were recruited; of these 154 were benign and 69 had differentiated thyroid cancer. We were able to detect driver mutation from plasma in 55 subjects (79.71%) of all malignant patients, and 11 patients in benign category had RAS mutation (follicular adenoma). Rest of the benign nodules did not have any detectable driver mutations. Conclusions and relevance: Plasma might be a viable noninvasive alternative source for detection of driver mutations (8-gene panel) in subjects with differentiated thyroid tumors and may have significant clinical utility.
MeSH term(s)	Humans ; Thyroid Nodule/diagnosis ; Thyroid Nodule/genetics ; Thyroid Nodule/pathology ; Neoplasm Recurrence, Local ; Thyroid Neoplasms/diagnosis ; Thyroid Neoplasms/genetics ; Thyroid Neoplasms/pathology ; Mutation ; Adenoma/pathology ; Proto-Oncogene Proteins B-raf/genetics
Chemical Substances	Proto-Oncogene Proteins B-raf (EC 2.7.11.1)
Language	English
Publishing date	2023-02-06
Publishing country	England
Document type	Journal Article
ZDB-ID	1183856-5
ISSN	1479-683X ; 0804-4643
ISSN (online)	1479-683X
ISSN	0804-4643
DOI	10.1093/ejendo/lvac018
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Article ; Online: Co-Regulation of Protein Coding Genes by Transcription Factor and Long Non-Coding RNA in SARS-CoV-2 Infected Cells: An In Silico Analysis.

Saha, Chinmay / Laha, Sayantan / Chatterjee, Raghunath / Bhattacharyya, Nitai P

Non-coding RNA

2021 Volume 7, Issue 4

Abstract: Altered expression of protein coding gene (PCG) and long non-coding RNA (lncRNA) have been identified in SARS-CoV-2 infected cells and tissues from COVID-19 patients. The functional role and mechanism (s) of transcriptional regulation of deregulated ... ...

Abstract	Altered expression of protein coding gene (PCG) and long non-coding RNA (lncRNA) have been identified in SARS-CoV-2 infected cells and tissues from COVID-19 patients. The functional role and mechanism (s) of transcriptional regulation of deregulated genes in COVID-19 remain largely unknown. In the present communication, reanalyzing publicly available gene expression data, we observed that 66 lncRNA and 5491 PCG were deregulated in more than one experimental condition. Combining our earlier published results and using different publicly available resources, it was observed that 72 deregulated lncRNA interacted with 3228 genes/proteins. Many targets of deregulated lncRNA could also interact with SARS-CoV-2 coded proteins, modulated by IFN treatment and identified in CRISPR screening to modulate SARS-CoV-2 infection. The majority of the deregulated lncRNA and PCG were targets of at least one of the transcription factors (TFs), interferon responsive factors (IRFs), signal transducer, and activator of transcription (STATs), NFκB, MYC, and RELA/p65. Deregulated 1069 PCG was joint targets of lncRNA and TF. These joint targets are significantly enriched with pathways relevant for SARS-CoV-2 infection indicating that joint regulation of PCG could be one of the mechanisms for deregulation. Over all this manuscript showed possible involvement of lncRNA and mechanisms of deregulation of PCG in the pathogenesis of COVID-19.
Language	English
Publishing date	2021-11-29
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2813993-8
ISSN	2311-553X ; 2311-553X
ISSN (online)	2311-553X
ISSN	2311-553X
DOI	10.3390/ncrna7040074
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Article: Decreased Levels of miR-126 and miR-132 in Plasma and Vitreous Humor of Non-Proliferative Diabetic Retinopathy Among Subjects with Type-2 Diabetes Mellitus.

Pramanik, Subhasish / Saha, Chinmay / Chowdhury, Subhankar / Bose, Chiranjit / Bhattacharyya, Nitai P / Mondal, Lakshmi Kanta

Diabetes, metabolic syndrome and obesity : targets and therapy

2022 Volume 15, Page(s) 345–358

Abstract: Purpose: Diabetic retinopathy (DR), the leading cause of blindness among working adults, is an urgent public health problem as diabetes mellitus (DM) is increasing at an alarming rate. Hyperglycemia-induced endothelial dysfunction is the principal ... ...

Abstract	Purpose: Diabetic retinopathy (DR), the leading cause of blindness among working adults, is an urgent public health problem as diabetes mellitus (DM) is increasing at an alarming rate. Hyperglycemia-induced endothelial dysfunction is the principal contributing factor leading to the development of microangiopathy. Altered levels of microRNA (miR), the negative regulator of protein-coding genes, have been observed and considered to be markers for DR. Present study aimed to find out whether miR levels in plasma could be effective biomarkers to differentiate between type 2 diabetes mellitus (T2DM) with non-proliferative retinopathy (NPDR) from T2DM with no-DR (DNR). Methods: We recruited 50 T2DM subjects comprising 31 NPDR and 19 DNR individuals. Surrogate markers of systemic oxidative stress and vascular endothelial growth factor (VEGF) were measured in plasma. Levels of miR-126 and miR-132 were determined in plasma and vitreous fluid using real-time PCR. Results: We observed that levels of miR-126 and miR-132 were decreased in NPDR subjects in comparison to DNR. Plasma levels of miRs were inversely correlated with secreted levels of VEGF and oxidative stress marker. The levels of these miRs showed discriminating ability between NPDR and DNR. Conclusion: Circulating miRs 126 and 132 in plasma or vitreous may serve as biomarkers for early diabetic retinopathy risk prediction, provided validated in a larger cohort and other forms of retinal vasculopathy or retinopathy in the future.
Language	English
Publishing date	2022-02-04
Publishing country	New Zealand
Document type	Journal Article
ZDB-ID	2494854-8
ISSN	1178-7007
ISSN	1178-7007
DOI	10.2147/DMSO.S346097
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Article ; Online: Plasma Cell-Free DNA to Differentiate Malignant from Benign Thyroid Nodules.

Dutta, Susmita / Tarafdar, Soham / Mukhopadhyay, Pradip / Bhattacharyya, Nitai P / Ghosh, Sujoy

The Journal of clinical endocrinology and metabolism

2021 Volume 106, Issue 5, Page(s) e2262–e2270

Abstract: Background: Molecular testing is increasingly used to identify malignancy in thyroid nodules (especially indeterminate category). Measurement of cell-free DNA (cfDNA) levels from plasma has been useful in diagnosis of cancers of other organs/tissues; ... ...

Abstract	Background: Molecular testing is increasingly used to identify malignancy in thyroid nodules (especially indeterminate category). Measurement of cell-free DNA (cfDNA) levels from plasma has been useful in diagnosis of cancers of other organs/tissues; herein we analyze cfDNA levels in patients with thyroid nodules to explore the possibility of establishing a cutoff for identification of malignancy. Methods: Patients underwent ultrasonography (USG) and USG-guided fine needle aspiration as well as surgery, where indicated. Cell-free DNA was extracted from plasma and quantified. In initial analysis (determination of cutoff), cfDNA levels were compared between Bethesda 2 and Bethesda 5 &6 to establish a cutoff value that could differentiate malignant from benign nodules. In the subsequent analysis, the aforementioned cutoff was applied (validation of cutoff) to those with indeterminate nodules to check ability to predict malignancy. Results: Fine needle aspiration (n = 119) yielded patients with Bethesda 2 (n = 69) Bethesda 5 & 6 (n = 13) who underwent histopathological confirmation. Cell-free DNA levels in these 2 groups were 22.85 ± 1.27 and 96.20 ± 8.31 (ng/mL) respectively. A cfDNA cutoff of 67.9 ng/mL, with area under the curve of 0.992 (95% CI, 0.97-1.0) with 100% sensitivity and 93% specificity was established to identify malignant lesions. Indeterminate group (Bethesda 3 & 4) underwent surgery (malignant n = 24), (benign n = 13), and using the previously identified cutoff for cfDNA, we were able to identify malignant lesions with a sensitivity of 100% and specificity of 92.3%. There was a very strong agreement between cfDNA-based classification with histopathology-based classification of benign and malignant nodules (Cohen's kappa 0.94; P < 0.001). Conclusion: Plasma cfDNA estimation could help differentiate malignant from benign thyroid nodules.
MeSH term(s)	Adenocarcinoma, Follicular/blood ; Adenocarcinoma, Follicular/diagnosis ; Adenocarcinoma, Follicular/pathology ; Adult ; Biopsy, Fine-Needle ; Cell-Free Nucleic Acids/analysis ; Cell-Free Nucleic Acids/blood ; Diagnosis, Differential ; Female ; Humans ; India ; Male ; Middle Aged ; Molecular Diagnostic Techniques/methods ; Molecular Diagnostic Techniques/standards ; Reference Values ; Thyroid Function Tests ; Thyroid Neoplasms/blood ; Thyroid Neoplasms/diagnosis ; Thyroid Neoplasms/pathology ; Thyroid Nodule/blood ; Thyroid Nodule/diagnosis ; Thyroid Nodule/pathology ; Young Adult
Chemical Substances	Cell-Free Nucleic Acids
Language	English
Publishing date	2021-01-21
Publishing country	United States
Document type	Journal Article ; Observational Study ; Research Support, Non-U.S. Gov't
ZDB-ID	3029-6
ISSN	1945-7197 ; 0021-972X
ISSN (online)	1945-7197
ISSN	0021-972X
DOI	10.1210/clinem/dgab030
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Article ; Online: Prevalence of non-diabetic kidney disease and inability of clinical predictors to differentiate it from diabetic kidney disease: results from a prospectively performed renal biopsy study.

Basu, Madhurima / Pulai, Smartya / Neogi, Subhasis / Banerjee, Mainak / Bhattacharyya, Nitai P / Sengupta, Sanghamitra / Mukhopadhyay, Pradip / Ray Chaudhury, Arpita / Ghosh, Sujoy

BMJ open diabetes research & care

2022 Volume 10, Issue 6

Abstract: Introduction: Renal involvement in type 2 diabetes mellitus (T2DM) may be due to diabetes (diabetic kidney disease (DKD)), causes other than diabetes (non-diabetic kidney disease (NDKD)) or overlap of DKD and NDKD (mixed kidney disease group). ... ...

Abstract	Introduction: Renal involvement in type 2 diabetes mellitus (T2DM) may be due to diabetes (diabetic kidney disease (DKD)), causes other than diabetes (non-diabetic kidney disease (NDKD)) or overlap of DKD and NDKD (mixed kidney disease group). Prevalence of NDKD and predictive value of clinical or biochemical indicators have been explored in retrospective cohorts with preselection biases warranting the need for prospectively conducted unbiased renal biopsy study. Research design and methods: Consecutive subjects aged >18 years with T2DM and renal involvement with estimated glomerular filtration rate of 30-60 mL/min/m Results: We screened 6247 subjects with T2DM of which 869 fulfilled inclusion criteria for biopsy. Of the 869 subjects, biopsy was feasible in 818 subjects. Out of 818, we recruited first 110 subjects who agreed to undergo renal biopsy. Among those 110 subjects, 73 (66.4%) had DKD; 20 (18.2 %) had NDKD; and 17 (15.4 %) had mixed kidney disease. Subjects with NDKD as compared with DKD had shorter duration of diabetes (p<0.001), absence of retinopathy (p<0.001) and absence of neuropathy (p<0.001). Logistic regression revealed that only presence of retinopathy and duration of diabetes were statistically significant to predict histopathological diagnosis of DKD. 30% of DKD did not have retinopathy, thereby limiting the utility of the same as a discriminator. Use of traditional indicators of biopsy would have indicated a need for renal biopsy in 87.2% of subjects, though 64.5% of the subjects had DKD, who would not have benefitted from biopsy. Conclusion: NDKD and mixed kidney disease in T2DM with renal involvement are very common and traditionally used parameters to select biopsies are of limited value in clinical decision making.
MeSH term(s)	Humans ; Diabetes Mellitus, Type 2/complications ; Diabetes Mellitus, Type 2/diagnosis ; Diabetes Mellitus, Type 2/epidemiology ; Prevalence ; Retrospective Studies ; Diabetic Nephropathies/diagnosis ; Diabetic Nephropathies/epidemiology ; Diabetic Nephropathies/etiology ; Biopsy/adverse effects ; Retinal Diseases/complications
Language	English
Publishing date	2022-12-14
Publishing country	England
Document type	Journal Article
ZDB-ID	2732918-5
ISSN	2052-4897 ; 2052-4897
ISSN (online)	2052-4897
ISSN	2052-4897
DOI	10.1136/bmjdrc-2022-003058
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Article ; Online: Chaperone protein HYPK interacts with the first 17 amino acid region of Huntingtin and modulates mutant HTT-mediated aggregation and cytotoxicity.

Choudhury, Kamalika Roy / Bhattacharyya, Nitai P

Biochemical and biophysical research communications

2015 Volume 456, Issue 1, Page(s) 66–73

Abstract: Huntington's disease is a polyglutamine expansion disorder, characterized by mutant HTT-mediated aggregate formation and cytotoxicity. Many reports suggests roles of N-terminal 17 amino acid domain of HTT (HTT-N17) towards subcellular localization, ... ...

Abstract	Huntington's disease is a polyglutamine expansion disorder, characterized by mutant HTT-mediated aggregate formation and cytotoxicity. Many reports suggests roles of N-terminal 17 amino acid domain of HTT (HTT-N17) towards subcellular localization, aggregate formation and subsequent pathogenicity induced by N-terminal HTT harboring polyQ stretch in pathogenic range. HYPK is a HTT-interacting chaperone which can reduce N-terminal mutant HTT-mediated aggregate formation and cytotoxicity in neuronal cell lines. However, how HYPK interacts with N-terminal fragment of HTT remained unknown. Here we report that specific interaction of HYPK with HTT-N17 is crucial for the chaperone activity of HYPK. Deletion of HTT-N17 leads to formation of tinier, SDS-soluble nuclear aggregates formed by N-terminal mutant HTT. The increased cytotoxicity imparted by these tiny aggregates might be contributed due to loss of interaction with HYPK.
MeSH term(s)	Amino Acid Sequence ; Animals ; Carrier Proteins/genetics ; Carrier Proteins/metabolism ; Cell Line ; Exons ; Gene Deletion ; Humans ; Huntingtin Protein ; Huntington Disease/metabolism ; Mice ; Microscopy, Confocal ; Molecular Chaperones/metabolism ; Molecular Sequence Data ; Mutation ; Nerve Tissue Proteins/genetics ; Peptides ; Protein Binding ; Protein Structure, Tertiary
Chemical Substances	Carrier Proteins ; HTT protein, human ; HYPK protein, mouse ; Huntingtin Protein ; Molecular Chaperones ; Nerve Tissue Proteins ; Peptides ; polyglutamine (26700-71-0)
Language	English
Publishing date	2015-01-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2014.11.035
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Article ; Online: Modulation of mutant Huntingtin aggregates and toxicity by human myeloid leukemia factors.

Banerjee, Manisha / Datta, Moumita / Bhattacharyya, Nitai P

The international journal of biochemistry & cell biology

2017 Volume 82, Page(s) 1–9

Abstract: Increased poly glutamine (polyQ) stretch at N-terminal of Huntingtin (HTT) causes Huntington's disease. HTT interacts with large number of proteins, although the preference for such interactions with wild type or mutated HTT protein remains largely ... ...

Abstract	Increased poly glutamine (polyQ) stretch at N-terminal of Huntingtin (HTT) causes Huntington's disease. HTT interacts with large number of proteins, although the preference for such interactions with wild type or mutated HTT protein remains largely unknown. HYPK, an intrinsically unstructured protein chaperone and interactor of mutant HTT was found to interact with myeloid leukemia factor 1 (MLF1) and 2 (MLF2). To identify the role of these two proteins in mutant HTT mediated aggregate formation and toxicity in a cell model, both the proteins were found to preferentially interact with the mutated N-terminal HTT. They significantly reduced the number of cells containing mutant HTT aggregates and subsequent apoptosis in Neuro2A cells. Additionally, in FRAP assay, mobile fraction of mutant HTT aggregates was increased in the presence of MLF1 or MLF2. Further, MLF1 could release transcription factors like p53, CBP and CREB from mutant HTT aggregates. Moreover, in HeLa cell co-expressing mutant HTT exon1 and full length MLF1, p53 was released from the aggregates, leading to the recovery of the expression of the GADD45A transcript, a p53 regulated gene. Taking together, these results showed that MLF1 and MLF2 modulated the formation of aggregates and induction of apoptosis as well as the expressions of genes indirectly.
MeSH term(s)	Animals ; Apoptosis ; Cell Line, Tumor ; Exons ; Fluorescence Recovery After Photobleaching ; Green Fluorescent Proteins/genetics ; Green Fluorescent Proteins/metabolism ; Humans ; Huntingtin Protein/antagonists & inhibitors ; Huntingtin Protein/chemistry ; Huntingtin Protein/genetics ; Huntingtin Protein/metabolism ; Huntington Disease/genetics ; Huntington Disease/metabolism ; Huntington Disease/pathology ; Mice ; Mutation ; Neurons/metabolism ; Neurons/pathology ; Nuclear Proteins/chemistry ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Peptide Fragments/chemistry ; Peptide Fragments/genetics ; Peptide Fragments/metabolism ; Peptides/chemistry ; Peptides/metabolism ; Protein Aggregation, Pathological/genetics ; Protein Aggregation, Pathological/pathology ; Protein Aggregation, Pathological/prevention & control ; Protein Interaction Domains and Motifs ; Proteins/chemistry ; Proteins/genetics ; Proteins/metabolism ; Recombinant Fusion Proteins/chemistry ; Recombinant Fusion Proteins/metabolism ; Recombinant Proteins/chemistry ; Recombinant Proteins/metabolism
Chemical Substances	HTT protein, human ; Huntingtin Protein ; MLF1 protein, human ; MLF2 protein, human ; Nuclear Proteins ; Peptide Fragments ; Peptides ; Proteins ; Recombinant Fusion Proteins ; Recombinant Proteins ; Green Fluorescent Proteins (147336-22-9) ; polyglutamine (26700-71-0)
Language	English
Publishing date	2017-01
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	1228429-4
ISSN	1878-5875 ; 1357-2725
ISSN (online)	1878-5875
ISSN	1357-2725
DOI	10.1016/j.biocel.2016.11.008
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Article: Huntington's disease: a monogenic disorder with cellular and biochemical complexities.

Bhattacharyya, Nitai P

The FEBS journal

2008 Volume 275, Issue 17, Page(s) 4251

MeSH term(s)	Humans ; Huntington Disease/genetics ; Huntington Disease/metabolism ; Huntington Disease/pathology
Language	English
Publishing date	2008-09
Publishing country	England
Document type	Comment ; Introductory Journal Article
ZDB-ID	2173655-8
ISSN	1742-4658 ; 1742-464X
ISSN (online)	1742-4658
ISSN	1742-464X
DOI	10.1111/j.1742-4658.2008.06560.x
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Article: In silico

Laha, Sayantan / Saha, Chinmay / Dutta, Susmita / Basu, Madhurima / Chatterjee, Raghunath / Ghosh, Sujoy / Bhattacharyya, Nitai P

Heliyon

2021 Volume 7, Issue 3, Page(s) e06395

Abstract: Altered expression of long noncoding RNA (lncRNA), longer than 200 nucleotides without potential for coding protein, has been observed in diverse human diseases including viral diseases. It is largely unknown whether lncRNA would deregulate in SARS-CoV-2 ...

Abstract	Altered expression of long noncoding RNA (lncRNA), longer than 200 nucleotides without potential for coding protein, has been observed in diverse human diseases including viral diseases. It is largely unknown whether lncRNA would deregulate in SARS-CoV-2 infection, causing ongoing pandemic COVID-19. To identify, if lncRNA was deregulated in SARS-CoV-2 infected cells, we analyzed in silico the data in GSE147507. It was revealed that expression of 20 lncRNA like MALAT1, NEAT1 was increased and 4 lncRNA like PART1, TP53TG1 was decreased in at least two independent cell lines infected with SARS-CoV-2. Expression of NEAT1 was also increased in lungs tissue of COVID-19 patients. The deregulated lncRNA could interact with more than 2800 genes/proteins and 422 microRNAs as revealed from the database that catalogs experimentally determined interactions. Analysis with the interacting gene/protein partners of deregulated lncRNAs revealed that these genes/proteins were associated with many pathways related to viral infection, inflammation and immune functions. To find out whether these lncRNAs could be regulated by STATs and interferon regulatory factors (IRFs), we used ChIPBase v2.0 that catalogs experimentally determined binding from ChIP-seq data. It was revealed that any one of the transcription factors IRF1, IRF4, STAT1, STAT3 and STAT5A had experimentally determined binding at regions within -5kb to +1kb of the deregulated lncRNAs in at least 2 independent cell lines/conditions. Our analysis revealed that several lncRNAs could be regulated by IRF1, IRF4 STAT1 and STAT3 in response to SARS-CoV-2 infection and lncRNAs might be involved in antiviral response. However, these in silico observations are necessary to be validated experimentally.
Language	English
Publishing date	2021-02-27
Publishing country	England
Document type	Journal Article
ZDB-ID	2835763-2
ISSN	2405-8440
ISSN	2405-8440
DOI	10.1016/j.heliyon.2021.e06395
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Article ; Online: Wnt signal transduction pathways: modules, development and evolution.

Nayak, Losiana / Bhattacharyya, Nitai P / De, Rajat K

BMC systems biology

2016 Volume 10 Suppl 2, Page(s) 44

Abstract: Background: Wnt signal transduction pathway (Wnt STP) is a crucial intracellular pathway mainly due to its participation in important biological processes, functions, and diseases, i.e., embryonic development, stem-cell management, and human cancers ... ...

Abstract	Background: Wnt signal transduction pathway (Wnt STP) is a crucial intracellular pathway mainly due to its participation in important biological processes, functions, and diseases, i.e., embryonic development, stem-cell management, and human cancers among others. This is why Wnt STP is one of the highest researched signal transduction pathways. Study and analysis of its origin, expansion and gradual development to the present state as found in humans is one aspect of Wnt research. The pattern of development and evolution of the Wnt STP among various species is not clear till date. A phylogenetic tree created from Wnt STPs of multiple species may address this issue. Results: In this respect, we construct a phylogenetic tree from modules of Wnt STPs of diverse species. We term it as the 'Module Tree'. A module is nothing but a self-sufficient minimally-dependent subset of the original Wnt STP. Authenticity of the module tree is tested by comparing it with the two reference trees. Conclusions: The module tree performs better than an alternative phylogenetic tree constructed from pathway topology of Wnt STPs. Moreover, an evolutionary emergence pattern of the Wnt gene family is created and the module tree is tallied with it to showcase the significant resemblances.
MeSH term(s)	Animals ; Evolution, Molecular ; Humans ; Models, Biological ; Phylogeny ; RNA, Ribosomal, 18S/genetics ; Wnt Signaling Pathway
Chemical Substances	RNA, Ribosomal, 18S
Language	English
Publishing date	2016-08-01
Publishing country	England
Document type	Journal Article
ISSN	1752-0509
ISSN (online)	1752-0509
DOI	10.1186/s12918-016-0299-7
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