RIMAL LAB
Rimal Lab research

p53, DRAM1 & autophagy

Rimal Lab

Stanford University

Welcome to our lab

Understanding how p53 programmes control autophagy, organelle contacts and stress responses

The laboratory concept focuses on mechanistic dissection of p53-regulated effectors (notably DRAM1), their roles in lysosomal and ER biology, and how those roles determine cell fate in stress or disease contexts.
Explore researchSelected publications

Principal investigator

Suman Rimal, PhD

Basic Life Research Scientist, Pathology

My work spans cell biology and translational models, with a focus on p53-regulated autophagy, organelle contacts and translational quality control. Publications include experimental and conceptual advances linking DRAM1 to ER stress and lysosome–ER contacts.
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Programmes

Current concept programmes

Key discovery linking p53-regulated DRAM1 to lysosome–ER contact and ER stress (figure from Wang et al., PNAS 2024).
01

DRAM1 and the p53–DRAM1 axis

How does p53-driven DRAM1 expression influence lysosomal function, organelle contacts and cell fate under genotoxic or mitochondrial stress?

Schematic and experimental evidence for p53-driven activation of autophagy and the role of DRAM1 (open-access review and experimental studies).
02

Autophagy (canonical and alternative) in p53-mediated cell fate decisions

How do p53 and its targets coordinate canonical and alternative autophagy pathways to decide between survival, repair or cell death?

Figure(s) from Nagata et al., 2015 (PMC4502683) showing DRAM1 subcellular localization to lysosomes and effects on autophagy — relevant to lysosome–ER contact and DRAM1-driven changes in organelle structure and calcium/ER stress biology.
03

Organelle contacts and calcium homeostasis: lysosome–ER communication

What are the molecular tethers that connect lysosomes and the ER, and how does p53/DRAM1 activity alter calcium signalling and ER stress?

Figure 6 from: "The p53 target DRAM1 modulates calcium homeostasis and ER stress by promoting contact between lysosomes and the ER through STIM1" (PNAS 2024). Shows DRAM1 perturbation of Ca2+ homeostasis and DRAM1–STIM1 interaction (confocal images, co‑IP and Fluo‑2 Ca2+ imaging) relevant to p53 downstream control of organelle contact sites, calcium signaling and stress responses.
04

Cell-cycle control and stress-response signalling downstream of p53

How do p53-regulated transcriptional programmes intersect with cell-cycle checkpoints and proteostasis pathways to determine proliferative decisions under stress?

Selected publications

Recent and defining work

2026

Dopamine-driven mitochondrial reverse electron transport in immune cells mediates gut-brain ROS signaling during sleep deprivation

Proceedings of the National Academy of Sciences

↗2024

The p53 target DRAM1 modulates calcium homeostasis and ER stress by promoting contact between lysosomes and the ER through STIM1

Proceedings of the National Academy of Sciences

↗2024

Stalled translation by mitochondrial stress upregulates a CNOT4-ZNF598 ribosomal quality control pathway important for tissue homeostasis

Nature Communications

↗2024

Ribosome stalling during c-myc translation presents actionable cancer cell vulnerability

PNAS Nexus

↗
2023

Reverse electron transfer is activated during aging and contributes to aging and age-related disease

EMBO Reports

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Opportunities

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