Dimple Notani

The paper identifies AR as the factor driving active enhancer resetting after transcriptional activation, which prevents transcriptional hyperactivation in ER-positive breast cancer.

The paper shows that eGATA3 mutations alter transcriptional regulation and lineage identity in luminal breast cancer without losing DNA-binding function.

The paper shows that enhancer activation during estrogen signaling indirectly represses neighboring non-target genes within the same TAD through dynamic chromatin interactions.

This study identifies drug-specific resistance mechanisms in ER+ breast cancer by analyzing multi-omic data, revealing distinct transcriptional and chromatin states associated with SERM, SERD, and ESR1 mutant resistance.

The paper develops a data-driven non-equilibrium model of chromatin polymer behavior, showing that active forces at specific scales explain anomalous fluctuations and 3D organization.

The paper investigates how centromere clustering states in Cryptococcus neoformans influence 3D genome architecture during the cell cycle, revealing unique organizational principles.

The paper identifies non-coding SNPs associated with prostate cancer risk in men of African ancestry using a deep learning model and experimental validation.

The paper shows that deleting Xist upstream sequences disrupts TAD organization, affects Xist expression, and leads to dysregulation of autosomal genes.

This paper shows that p53 loss in colorectal cancer increases enhancer activity, drives oncogenic pathways, and correlates with poor survival in p53-deficient tumors.

This study shows hypoxia-induced CTCF promotes EMT in breast cancer by regulating alternative splicing through chromatin looping and RNA Pol II pausing.

The paper identifies nuclear myosin I as a regulator of estrogen receptor-α clustering on enhancers, showing that this clustering is not essential for robust transcriptional responses to estrogen.

The paper shows that paused RNA polymerase II enhances transcription factor binding through RNA-dependent mechanisms, leading to stronger transcriptional activation upon release.

This study shows that RNA binding enhances estrogen receptor-alpha (ER) chromatin binding, which limits its transcriptional activation in response to estrogen.

This study shows that H3S10 phosphorylation during mitosis preserves chromatin domain and promoter identity by compacting active regions and stabilizing nucleosomes, ensuring proper transcriptional reactivation in the next interphase.

This study examines how HPV integration affects host chromatin structure and gene regulation in cervical cancer, finding that integrations are enriched in active chromatin regions and induce local and long-range transcriptional upregulation within TADs.

The paper shows that CTCF/cohesin binding during DNA replication causes replication stress and genomic instability at CBSs in cancer.

The paper reports genomic surveillance of SARS-CoV-2 in Bengaluru, India, across three pandemic waves, identifying 18 clades and 196 lineages, with Delta dominant in the second wave and Omicron BA.2 dominant in the third.

The paper shows boundary-associated RNAs enhance TAD insulation by promoting CTCF clustering at TAD boundaries.

The paper shows that IP3/Ca2+ signals in specific neurons drive dSET2 expression, which regulates gene expression through H3K36 methylation to enable pupariation under protein deficiency.

The paper shows that unliganded ERα pre-marks enhancer sites, which form 3D clusters upon ligand exposure, driving transient gene expression.