Intracellular Ion Channels Laboratory

12/29/2025

As we step into 2026, I’m grateful to my lab members, who continue to be gladiators in lab coats, fearless, resilient, and relentlessly curious. This past year was one of our most productive yet. We pushed boundaries, asked bold questions, and turned ideas into discoveries.
We are thankful to AHA, NCATS and NHLBI for their long lasting support.

12/29/2025

Collaborated with Prof Rajaram on

Pseudomonas aeruginosa EVs Drive Cardiac Dysfunction During Infection. mBio.

This work demonstrates that extracellular vesicles (EVs) released by Pseudomonas aeruginosa are potent mediators of infection‑induced cardiac dysfunction.

Pseudomonas aeruginosa (P.a.) is a gram-negative, opportunistic bacterium abundantly present in the environment. Often P.a. infections cause severe pneumonia, if left untreated. Surprisingly, up to 30% of patients admitted to the hospital for community- acquired pneumonia develop...

12/29/2025

Worked with Prof Patel to study zyxin

Zyxin Binds Chromosomal DNA and Links to Mitochondrial Integrity. Biochemistry and Cell Biology.

This paper uncovers a surprising nuclear role for zyxin, traditionally known as a cytoskeletal protein.

Human zyxin is a key component of the focal adhesion complex, playing a role in mediating cell–cell adhesion and cytoskeletal dynamics. Moreover, zyxin shuttles between the cytoplasm and the nucleus, where it contributes to regulating gene expression. Although identified over 30 years ago, zyxin.....

12/29/2025

Assisted Dr Nuo Sun for

Mitophagy Protects Against FAO‑Deficient Cardiomyopathy. Nature Communications.

This study reveals that mitophagy acts as a compensatory survival mechanism in cardiomyopathy caused by defective mitochondrial fatty‑acid β‑oxidation.

The heart relies on fatty acid oxidation as its main energy source. Here they show that impaired fatty acid metabolism disrupts mitophagy in the heart and that enhancing mitophagy via USP30 inhibition can restore heart function in models of fatty acid oxidation deficiency.

12/29/2025

Worked with Prof. Terentyev for

Enhancing SK Channels Suppresses Ventricular Arrhythmias. Circulation Research.

In a mouse model of catecholaminergic polymorphic ventricular tachycardia (CPVT), this study shows that pharmacological activation of small‑conductance Ca²⁺‑activated K⁺ (SK) channels stabilizes cardiac electrical activity and prevents lethal arrhythmias.

BACKGROUND: Sarcolemmal small conductance Ca2+-activated K+ channels have the unique capacity to translate intracellular Ca2+ signal into repolarization, while mitochondrial SK channels can link Ca2+ cycling to mitochondrial function. We hypothesize that pharmacological enhancement of SK channels ca...

12/29/2025

We assisted Prof Christian

CLIC1 Is Essential for Microglial Morphodynamics and Neuroinflammation. Science Advances

This paper demonstrates that CLIC1 is a critical regulator of microglial shape, motility, and inflammatory activation.

CLIC1 regulates surveillance, morphology, and interleukin release in mouse and human brain microglia.

12/29/2025

We assisted Prof Jahani-Asl for

OSMR–CLIC1 Crosstalk in Glioblastoma. Accepted in Signal Transduction and Targeted Therapy.

This study uncovers a previously unrecognized signaling axis between oncostatin M receptor (OSMR) and CLIC1, revealing that their molecular crosstalk fuels several hallmark oncogenic pathways in glioblastoma.

12/29/2025

We followed up MAM Cl channels as well

Biophysical characterization of anion channels in Mitochondrion–Endoplasmic‑Reticulum Contact sites (MERCs). Biophysical Journal.
This work provides the first detailed biophysical analysis of anion channel activity at MERCs, the critical microdomains where mitochondria and ER membranes physically and functionally interact.

The mitochondrion-endoplasmic reticulum (ER) contact sites (MERCs, also known as mitochondrial-associated membranes [M**s]) are specialized regions of the ER that are in close proximity to the mitochondrion. These organelle structures play essential roles in a variety of processes, such as calcium s...

12/29/2025

The first paper was

Functional large-conductance calcium and voltage-gated potassium channels in extracellular vesicles act as gatekeepers of structural and functional integrity. Nature Communications. This study uncovers a surprising and elegant layer of cellular regulation: extracellular vesicles (EVs) carry fully functional BK (large‑conductance Ca²⁺‑ and voltage‑activated K⁺) channels.

Extracellular vesicles secreted by cells play a crucial role in cellular communication. Here, the authors identify a functional BK channel in extracellular vesicle membranes and establish its role in preserving vesicle integrity, K+ homeostasis, and physiological function.

03/20/2025

https://academic.oup.com/eurjpc/advance-article/doi/10.1093/eurjpc/zwaf137/8087961?login=true

Ragavendra R Baliga, Harpreet Singh, Jagat Narula; Sodium or Potassium, and Chloride or Bicarbonate: Which Combination is Worth Its Salt?, European Journal

01/07/2025

Behind the paper story

Extracellular vesicles (EVs or exosomes) must maintain their ionic homeostasis during intercellular transport by activating ion channels and transporters to avoid osmotic shock. We have identified the first functional ion channel in EVs responsible for maintaining potassium homeostasis.

01/07/2025

Our group just published

Extracellular vesicles secreted by cells play a crucial role in cellular communication. Here, the authors identify a functional BK channel in extracellular vesicle membranes and establish its role in preserving vesicle integrity, K+ homeostasis, and physiological function.