Eunus S. Ali, Ph.D.

PFKM governs metabolic shifts throughout skeletal muscle differentiation - Nature Metabolism Subcellular compartmentalization of the glycolytic enzyme PFKM regulates cell fate and metabolic switch during skeletal muscle differentiation.

www.nature.com/articles/s42...

YBX1&YBX3 as novel targets to potentiate immune checkpoint blockade response in gliomas AbstractBackground. Glioblastoma (GBM) exhibits profound resistance to CD8⁺ T cell-mediated killing, yet the tumor-intrinsic mechanisms driving this immune

A new Neuro-Oncology study YBX1&YBX3 as Novel Targets to Potentiate Immune Checkpoint Blockade Response in Gliomas has been published. Crismita Dmello, PhD, is the senior author of this study, and Heba Ali, PhD, a postdoc from the Dmello Lab. academic.oup.com/neuro-oncolo...

JCI Insight - Palmitate impairs autophagic degradation via oxidative stress/perilysosomal Ca2+ overload/mTORC1 activation pathway in pancreatic β cells insight.jci.org/articles/vie...

The mTORC1-SLC4A7 axis stimulates bicarbonate import to enhance de novo nucleotide synthesis Ali et al. showed that bicarbonate (HCO3−) is a limiting substrate for nucleotide synthesis in proliferating cells. In response to growth factor stimuli, the mTORC1-S6K-eIF4B axis promotes an increase...

Reposted: Cellular bicarbonate is historically known to scientists as a pH regulator or a metabolic bi-product. Our study represents the first indication that bicarbonate, similar to glutamine or aspartate, can have anabolic properties in case of cancer cell growth. www.cell.com/molecular-ce...

Glyceraldehyde-3-phosphate dehydrogenase homologs as bifunctional gatekeepers of metabolic segregation in Pseudomonas putida | PNAS Metabolically versatile Pseudomonas species can assimilate various glycolytic and gluconeogenic substrates. Simultaneous assimilation is known to s...

A really cool study: >> Glyceraldehyde-3-phosphate dehydrogenase homologs as bifunctional gatekeepers of metabolic segregation in Pseudomonas putida | PNAS www.pnas.org/doi/10.1073/...

📢ATTENTION BSKY COMMUNITY - We are expanding!! If you are interested in studying metabolic drivers of cancer progression and therapy resistance using bioengineered models consider joining our group at the Moffitt! Pl. repost, tks

moffitt-cancer-center-careers.hctsportals.com/jobs/2115134...

This beautiful collaborative article has shown that PLK1, via regulation of serine metabolism, promotes sphingolipid biosynthesis in prostate cancer models.

www.biorxiv.org/content/10.1...

This beautiful collaborative article has shown that PLK1, via regulation of serine metabolism, promotes sphingolipid biosynthesis in prostate cancer models.

www.biorxiv.org/content/10.1...

NUDT5 regulates purine metabolism and thiopurine sensitivity by interacting with PPAT Cells generate purine nucleotides through de novo purine biosynthesis (DNPB) and purine salvage. Purine salvage represses DNPB to prevent excessive purine nucleotide synthesis through mechanisms that ...

NUDT5 regulates purine metabolism and thiopurine sensitivity by interacting with PPAT | Science www.science.org/doi/10.1126/...

Calcium Signaling As a Therapeutic Target for Liver Steatosis Hepatic steatosis, the first step in nonalcoholic fatty liver disease (NAFLD), can arise from various pathophysiological conditions. While lipid metab…

How Excessive Lipid Droplet Accumulation Alters Liver Function: www.sciencedirect.com/science/arti...

Evidence for the interaction of peroxiredoxin-4 with the store-operated calcium channel activator STIM1 in liver cells Ca2+ entry through store-operated Ca2+ channels (SOCs) in the plasma membrane (PM) of hepatocytes plays a central role in the hormonal regulation of l…

www.sciencedirect.com/science/arti...

Deranged hepatocyte intracellular Ca2+ homeostasis and the progression of non-alcoholic fatty liver disease to hepatocellular carcinoma Hepatocellular carcinoma (HCC) is the second leading cause of cancer-related deaths in men, and the sixth in women. Non-alcoholic fatty liver disease …

www.sciencedirect.com/science/arti...

This small study has been kind of seminal and probably, a landmark study. Low intracellular calcium generates more lipid droplets in cytoplasm :-(. Lots of high-profile papers came out from different lab based on this discovery. portlandpress.com/biochemj/art...

JCI - RSK1-driven TRIM28/E2F1 feedback loop promotes castration-resistant prostate cancer progression www.jci.org/articles/vie...

About twenty calcium signaling proteins were identified, including those involved in regulating calcium concentrations in the cytoplasm, endoplasmic reticulum and mitochondria.

www.mdpi.com/2072-6694/12...

www.mdpi.com/2072-6694/12...

I'm extremely thrilled to announce that I will be starting as a group leader at Stanford this upcoming fall! My lab will be studying how RNAs exert themselves in the cell to induce a multitude of biological phenomena using ML, cryoEM/ET, and biochemistry!

www.yousufakhan.com

Ribonucleotide reductase regulatory subunit M2 drives glioblastoma TMZ resistance through modulation of dNTP production Ribonucleotide reductase subunit M2-mediated dGTP and dCTP production promotes resistance to standard-of-care chemotherapy in GBM.

Ribonucleotide reductase regulatory subunit M2 drives glioblastoma TMZ resistance through modulation of dNTP production | Science Advances www.science.org/doi/full/10....

Impaired Ca2+ signaling due to hepatic steatosis mediates hepatic insulin resistance in Alström syndrome mice that is reversed by GLP-1 analog treatment | American Journal of Physiology-Cell Physiology | American Physiological Society Ca2+ signaling plays a critical role in the regulation of hepatic metabolism by hormones including insulin. Changes in cytoplasmic Ca2+ regulate synthesis and posttranslational modification of key signaling proteins in the insulin pathways. Emerging evidence suggests that hepatocyte intracellular Ca2+ signaling is altered in lipid-loaded liver cells isolated from obese rodent models. The mechanisms of altered Ca2+-insulin and insulin-Ca2+ signaling pathways in obesity remain poorly understood. Here, we show that the kinetics of insulin-initiated intracellular (initial) Ca2+ release from endoplasmic reticulum is significantly impaired in steatotic hepatocytes from obese Alström syndrome mice. Furthermore, exenatide, a glucagon-like peptide-1 (GLP-1) analog, reversed lipid-induced inhibition of intracellular Ca2+ release kinetics in steatotic hepatocytes, without affecting the total content of intracellular Ca2+ released. Exenatide reversed the lipid-induced inhibition of intracellular Ca2+ release, at least partially, via lipid reduction in hepatocytes, which then restored hormone-regulated cytoplasmic Ca2+ signaling and insulin sensitivity. This data provides additional evidence for the important role of Ca2+ signaling pathways in obesity-associated impaired hepatic lipid homeostasis and insulin signaling. It also highlights a potential advantage of GLP-1 analogs when used to treat type 2 diabetes associated with hepatic steatosis.

journals.physiology.org/doi/full/10....

doi.org/10.1016/j.mo...

Calcium Signaling As a Therapeutic Target for Liver Steatosis Hepatic steatosis, the first step in nonalcoholic fatty liver disease (NAFLD), can arise from various pathophysiological conditions. While lipid metabolism in the liver is normally balanced such that ...

Calcium Signaling As a Therapeutic Target for Liver Steatosis: Trends in Endocrinology & Metabolism www.cell.com/trends/endoc...

Deranged hepatocyte intracellular Ca2+ homeostasis and the progression of non-alcoholic fatty liver disease to hepatocellular carcinoma Hepatocellular carcinoma (HCC) is the second leading cause of cancer-related deaths in men, and the sixth in women. Non-alcoholic fatty liver disease …

www.sciencedirect.com/science/arti...

Calcium Signaling As a Therapeutic Target for Liver Steatosis Hepatic steatosis, the first step in nonalcoholic fatty liver disease (NAFLD), can arise from various pathophysiological conditions. While lipid metabolism in the liver is normally balanced such that ...

Calcium Signaling As a Therapeutic Target for Liver Steatosis: Trends in Endocrinology & Metabolism www.cell.com/trends/endoc...

Calcium Signaling As a Therapeutic Target for Liver Steatosis Hepatic steatosis, the first step in nonalcoholic fatty liver disease (NAFLD), can arise from various pathophysiological conditions. While lipid metabolism in the liver is normally balanced such that ...

Calcium Signaling As a Therapeutic Target for Liver Steatosis: Trends in Endocrinology & Metabolism www.cell.com/trends/endoc...

Regulation of nucleotide metabolism in cancers and immune disorders Nucleotides are the fundamental building blocks for the preservation of life. As monomeric units, purine and pyrimidine nucleotides are polymerized into RNA and DNA. Mammalian cells require extracellu...

Regulation of nucleotide metabolism in cancers and immune disorders: Trends in Cell Biology www.cell.com/trends/cell-...

So grateful and excited to partner with the Stephenson Global Pancreatic Cancer Research Institute to advance our collaborative program targeting lysosome and Kras metabolism in pancreatic cancer!

michmed.org/rwVDK

Targeting cardiometabolic risk in type 1 diabetes through incretin physiology People living with type 1 diabetes have significantly increased cardiovascular risk compared with the general population. Traditional risk factors include hypertension, dyslipidaemia, and obesity. How...

Targeting cardiometabolic risk in type 1 diabetes through incretin physiology: Trends in Endocrinology & Metabolism www.cell.com/trends/endoc...

Itaconate promotes inflammatory responses in tissue-resident alveolar macrophages and exacerbates acute lung injury Shan et al. demonstrate that itaconate promotes proinflammatory cytokine production and NLRP3 inflammasome activation in alveolar macrophages, contrasting its anti-inflammatory role in BMDMs. Itaconat...

We used to know itaconate is an anti-inflammatory metabolite; but this article argues it can also act as pro-inflammatory in some situations: www.cell.com/cell-metabol...

Mitochondria complex III–generated superoxide is essential for IL-10 secretion in macrophages Mitochondrial ROS is necessary for the release of a critical anti-inflammatory cytokine.

Mitochondria complex III–generated superoxide is essential for IL-10 secretion in macrophages | Science Advances www.science.org/doi/10.1126/...