Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Sequence-to-expression approach to identify etiological non-coding DNA variations in P53 and cMYC-driven diseases.

Human molecular genetics - 19 Sept 2024

Kin Katherine, Bhogale Shounak, Zhu Lisha, Thomas Derrick, Bertol Jessica, Zheng W Jim, Sinha Saurabh, Fakhouri Walid D

Abstract excerpt

Disease risk prediction based on genomic sequence and transcriptional profile can improve disease screening and prevention. Despite identifying many disease-associated DNA variants, distinguishing deleterious non-coding DNA variations remains poor for most common diseases. In this study, we designed in vitro experiments to uncover the significance of occupancy and competitive binding between P53 and cMYC on...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Binding Sites
Share to Cell Line, Tumor

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Doxorubicin

Share to Polymorphism, Single Nucleotide

Share to Protein Binding

Share to Proto-Oncogene Proteins c-myc

Share to Tumor Suppressor Protein p53

Source

Open in PubMed Open full text

Identifiers

PMID: 39017605
DOI: 10.1093/hmg/ddae109
PMCID: PMC11413647

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Sequence-to-expression approach to identify etiological non-coding DNA variations in P53 and cMYC-driven diseases.PMID 39017605Read ↗

Sequence-to-expression approach to identify etiological non-coding DNA variations in P53 and cMYC-driven diseasesSemantic proximity Read ↗

Sequence-to-expression approach to identify etiological non-coding DNA variations in P53 and cMYC-driven diseasesSemantic proximity Read ↗

The effect of non-coding DNA variations on P53 and cMYC competitive inhibition at cis-overlapping motifs.Semantic proximity Read ↗

Revealing a human p53 universeSemantic proximity Read ↗

MOCCS profile analysis clarifies the cell type dependency of transcription factor-binding sequences and cis-regulatory SNPs in humansSemantic proximity Read ↗

Saturation mutagenesis of disease-associated regulatory elementsSemantic proximity Read ↗

Machine Learning Prediction of Non-Coding Variant Impact in Human Retinal <i>Cis</i> -Regulatory ElementsSemantic proximity Read ↗

Overlapping binding sites underlie TF genomic occupancySemantic proximity Read ↗

Machine Learning Prediction of Non-Coding Variant Impact in Human Retinal cis -Regulatory ElementsSemantic proximity Read ↗

Transcription factor-binding k-mer analysis clarifies the cell type dependency of binding specificities and cis-regulatory SNPs in humans.Semantic proximity Read ↗

Comparative analysis of models in predicting the effects of SNPs on TF-DNA binding using large-scale in vitro and in vivo data.Semantic proximity Read ↗

Codebook: sequence specificity and genomic binding of poorly-characterized human transcription factorsSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.