Vikram R. Paralkar

This study shows that the myeloid transcription factor CEBPA accelerates RNA Polymerase I dynamics at rDNA repeats by modulating promoter escape, Pol I accumulation, and DNA supercoiling resolution.

This study shows that impaired 5'ETS pre-rRNA cleavage disrupts nucleolar organization, leading to mislocalization of RNA and proteins, and broader nuclear architecture changes.

The paper examines rRNA transcription and abundance in normal and leukemic hematopoiesis, finding cell-type-specific variations and functional roles in myeloid differentiation.

The paper compares transcriptomes and chromatin accessibility in MEP, ERY, and MEG cells to reveal divergence in gene regulation during differentiation.

This study identifies PHF6 and PHIP as a chromatin complex that represses AML stemness, showing their functional relationship and the impact of their mutations.

This study shows that PHF6 loss increases AML aggressiveness by enhancing leukemia stem cell self-renewal through context-specific transcriptional changes.

The paper benchmarks six MYB inhibitors using a nascent transcriptomics assay, revealing partial specificity, off-target activity, and mixed agonism-antagonism effects.

The paper reconstructs a sparsely interconnected transcriptional hierarchy in leukemia cells stabilized by incoherent feed-forward loops and shows inhibitors disrupt core regulators' programs.

The paper customizes genome assemblies for rDNA mapping in human and mouse by masking repetitive regions and adding reference sequences, enabling better analysis of rDNA-binding factors.

The paper identifies cell-type-specific transcription factors that bind rDNA and regulate rRNA transcription, showing CEBPA's role in promoting Pol I occupancy and rRNA synthesis in myeloid progenitors.

The paper identifies transcription factors regulating MHC-II expression in AML and shows their role in immune evasion and relapse.

The paper identifies a modular core regulatory circuitry in AML that enforces oncogene expression in KMT2A-rearranged leukemias.