Divine Aleru, Microbiome Signatures Research Coordinator

This study explores how dietary magnesium levels affect the gut microbiota of rats. It shows that low magnesium increases beneficial microbes, while high magnesium promotes potentially harmful bacteria. These changes may influence metabolism and gut health.

This study explores the conditions that regulate C. difficile spore germination in the GI tract, showing how pH, bile salts, calcium, and amino acids interact to trigger germination, and how this affects C. difficile infection risk.

The study investigates Streptococcus pneumoniae’s virulence, immune evasion strategies, and how aging impacts susceptibility to infections. It explores diagnostic and vaccine strategies for improving prevention in high-risk groups.

Fungal competition for magnesium between Candida albicans and Pseudomonas aeruginosa significantly lowers bacterial fitness but enhances resistance to polymyxin antibiotics. This highlights the role of Mg²⁺ in microbial interactions and offers potential therapeutic avenues to manage polymicrobial infections and combat antibiotic resistance.

This study identifies MpfA (SA0657) as a key magnesium protection factor in Staphylococcus aureus. Disabling MpfA makes the bacterium highly sensitive to Mg2+ and pinpoints a conserved CBS-domain residue needed for function, supporting a role in Mg2+ export or detoxification.

This study shows that the Salmonella peptide MgtR directly limits the MgtA magnesium transporter during Mg2+ starvation. Deleting mgtR raises MgtA protein levels and makes MgtA appear earlier, which improves growth in low magnesium when other transporters are absent.

This study shows that the magnesium transporter MgtE suppresses Pseudomonas aeruginosa type III secretion by blocking ExsA translation. MgtE activates the GacAS system, increases rsmY and rsmZ, and limits ExsA production, which lowers T3SS gene transcription without reducing exsA mRNA.

What was studied?This experimental study investigated how the bacterial magnesium transporter A (MgtA) functions at the biochemical level and how membrane lipids and free magnesium concentrations regulate its activity. The authors focused on MgtA from Escherichia coli as a model system to clarify how this transporter responds to magnesium limitation and how it integrates environmental […]

This review explains how hosts restrict pathogens by triggering magnesium limitation signals during infection. It shows that bacteria respond to what they feel inside their cytoplasm and highlights Salmonella’s need for Mg2+ transport systems and stress sensors to survive inside macrophages.

This review explains that the small intestine absorbs magnesium through regulated transcellular and paracellular pathways. Hormones, luminal pH sensing, and proton pump inhibitors can suppress absorption, while fermentation-linked acidification may support uptake. It links dysbiosis and inflammation to impaired magnesium bioavailability.

This review explains how magnesium imbalance affects neuromuscular and cardiac function and why lab results can mislead. It highlights pre-analytical errors, limits of serum magnesium, and strong links between magnesium, potassium, calcium, and gut-related absorption or loss.

This mini-review explains how higher-dose magnesium can reduce bacterial adhesion and weaken biofilm formation. It highlights why biofilms resist cleaning and heat, and it summarizes evidence that magnesium in milk can reduce Bacillus biofilms and lower survival after pasteurization.

This study shows that low gut magnesium activates a virulence pathway in EHEC O157:H7 that boosts LEE gene expression and intestinal attachment. A magnesium-rich diet raised colon magnesium and sharply reduced bacterial adherence in mice, supporting magnesium as an anti-virulence approach.

This review explains how magnesium, zinc, copper, iron, and selenium shape innate and adaptive immunity and long-term inflammation. It highlights that magnesium deficiency can weaken the gut barrier and reduce bifidobacteria, which can raise inflammatory cytokines and worsen immune balance.

This review explains how bacteria sense magnesium outside and inside the cell, switch among Mg2+ transporters, and remodel their envelope to survive low Mg2+. It shows how Mg2+ limitation and host stresses can activate virulence programs, especially in Salmonella and related pathogens.

This review explains how magnesium supports energy, vascular tone, glucose handling, bone strength, and brain excitability, and why low intake or poor absorption can raise chronic disease risk. It also clarifies why serum magnesium can miss deficiency and why gut factors matter for magnesium availability.

This review explains how magnesium supports energy, vascular function, immunity, glucose control, bone strength, and muscle health, and how low intake or poor absorption can raise risks for cardiometabolic disease and inflammation. It also highlights gut factors that may reduce magnesium availability.

Magnesium (Mg) is a vital metal that not only supports critical cellular functions in both humans and microbes but also plays a significant role in shaping microbial pathogenesis. By regulating microbial growth, virulence factor expression, and competition for nutrients, magnesium directly influences infection outcomes. Understanding how magnesium interacts with microbial communities and the host immune system provides novel insights into therapeutic strategies that modulate microbial behavior, potentially improving infection management and microbiome health.

This review explains how dietary pectin may shift gut microbiota and SCFA production to shape allergy risk, while also noting reports of pectin-related sensitization and anaphylaxis. It highlights structure-dependent microbial associations and immune pathways that matter in asthma and food allergy.

This review explains how thiol-based chelators bind mercury, cadmium, and lead and how that chemistry guides clinical treatment. It compares common agents such as DMSA and DMPS, outlines safety tradeoffs, and clarifies why brain and intracellular metal stores remain hard to remove.

This study shows the gut microbiome helps clear dietary methylmercury by demethylating it in the intestine. People differed widely in elimination rates, which tracked with stool demethylation activity and specific taxa patterns, especially Alistipes.

This pilot study in late pregnancy linked maternal gut microbiota to mercury biomarkers and tested whether microbes directly change stool methylmercury. Stool methylmercury did not predict fetal exposure, and mercury cycling genes were largely absent, suggesting indirect microbiome pathways may matter more.

This review explains how mercury form and exposure route change diagnosis and treatment. It compares blood, urine, and hair biomarkers, discusses why symptoms do not always match measured levels, and summarizes supportive care and chelation options while noting that firm treatment thresholds remain hard to define.

This review explains how workplace microbes, chemicals, metals, and air pollution can change the adult human microbiome. It highlights links to colonization, gut permeability, and immune effects, and it suggests that stopping exposure alone may not reverse risk if microbiome changes persist.

Mercury pollution reshaped a soil microbiome by lowering alpha diversity and increasing between-community divergence. A focal Pseudomonas strain survived mercury stress by acquiring mercury resistance, and conjugative elements spread merA widely across taxa, showing how toxicants can drive community change and resistance gene flow.

This study shows human gut microbiota can demethylate methylmercury and that detox rates vary by exposure level and food source. Higher Desulfovibrio and methanogen signals aligned with faster demethylation, while mer and hgcAB genes did not explain the process.

Mercury-contaminated paddy soil increased plant and human pathogen signals under both ambient and elevated CO₂. Metagenomics showed strong activation of efflux pumps, especially the RND family, alongside higher adherence and secretion-related virulence factors, linking metal exposure to antibiotic resistance potential and pathogen aggressiveness.

This study shows that trace mercury exposure can favor the USA300-LV MRSA lineage in South America. Mercury reverses the fitness cost of COMER, helps USA300-LV outcompete other strains, and increases expression of major virulence genes under sub-inhibitory mercury.

This review explains how methylmercury forms in the environment, enters the body, and reaches the brain through fast “exchange” chemistry with sulfur and selenium groups. It highlights microbial methylation as the exposure driver and selenoenzymes as vulnerable targets that amplify neurotoxicity.

This study shows mercury(II) can bind histidines to inhibit chymotrypsin and trigger irreversible denaturation and aggregation. Imidazole blocks aggregation, aggregation rises above pH 6.5, and histidine-targeting DEPC shifts mercury effects, supporting a two-histidine mechanism.

This review explains how mercury, cadmium, arsenic, and lead disrupt glutathione and cysteine-based defenses. It emphasizes catalytic mercury-driven glutathione oxidation and metal-conjugate breakdown that generates electrophiles and metal sulfides, linking these mechanisms to kidney, neurologic, and carcinogenic injury patterns.

This study shows that mussel metallothionein binds mercury in two main forms: a dominant linear Hg–thiolate complex and a substantial clustered Hg–thiolate structure with Hg–Hg pairing. The clustered form likely concentrates in the α-domain and supports cellular mercury detoxification.

What was studied?This original research study used large-scale bioinformatics to map where mercury detoxification genes occur across prokaryotes and to infer how those genes evolved. The authors screened 84,032 bacterial and archaeal genomes, including isolate genomes, metagenome-assembled genomes, and single-cell genomes, for mercuric reductase (MerA), which reduces Hg(II) to volatile Hg(0), and organomercury lyase (MerB), […]

What was reviewed?This review explained how mercury cycles through air, water, and soil and how microbes control key steps that change mercury toxicity. It focused on mercury-resistant bacteria and the mer operon as a practical framework for understanding detoxification and resistance. The authors also compared physical and chemical cleanup approaches with biologic approaches, arguing that […]

This review explains how mercury-tolerant bacteria, fungi, and microalgae resist and transform mercury. It highlights detox genes such as the mer system, biofilm binding, and redox-driven methylation and demethylation that change mercury toxicity and exposure risk across ecosystems.

This review explains that mercury toxicity largely comes from binding thiol groups in cysteine, glutathione, and proteins. That binding disrupts enzymes, antioxidant defenses, and signaling, driving oxidative stress, mitochondrial injury, and multi-organ effects that may also influence gut barrier stress and downstream microbiome function.

This study shows that methylmercury delivered as a cysteine complex increases liver and mitochondrial mercury uptake and worsens mitochondrial stress. Methionine pre-treatment lowers mercury uptake, preserves oxygen use, and protects mitochondrial function and cell viability in rat liver slices.

This study shows that mercury cysteine conjugates act like amino acids and directly affect sulfur metabolism enzymes. Human GTK can use and inhibit these conjugates, while cystathionine γ-lyase is irreversibly inactivated at low micromolar mercury levels, expanding how mercury can drive toxicity.

This review explains how inorganic mercury and methylmercury enter the gut, kidney, liver, brain, and placenta by binding to thiols and mimicking nutrients that use amino acid and organic anion transporters, which helps predict where mercury accumulates and how chelators enhance excretion.

This study shows that low, environmentally relevant mercury levels can boost plasmid transfer of antibiotic resistance genes between E. coli by driving oxidative stress, membrane damage, and transfer-gene activation, while very high mercury levels suppress transfer by harming cells.

This study measured mercury in urine and hair in dental workers and controls and linked urine mercury to the number of amalgam fillings. Levels stayed below occupational limits, but fillings still acted as a steady exposure source.

This review explains how inorganic and methylmercury disrupt gut microbes, metabolites, tight junctions, and immune signals, making the gut a key target tissue that can drive liver and brain toxicity through gut–liver and gut–brain pathways.

This review explains how heavy metals and microplastics work together to drive antimicrobial resistance by enriching biofilms, speeding gene transfer, and co-selecting metal and antibiotic resistance in soil and water microbiomes, creating environmental reservoirs that can feed resistant pathogens into humans.

Mercury primarily affects microbiome pathogenesis by acting as a strong toxic selector that enriches organisms carrying mercury detox systems and the mobile elements that often co-carry antimicrobial resistance. In the gut, mercury speciation and bioavailability are shaped by thiols and sulfide chemistry, while microbial responses are dominated by the mer operon toolkit that detects Hg(II), traffics it intracellularly, and reduces it to Hg(0) for detox and loss from the cell.

This review explains how gut microbes influence ferroptosis in colorectal cancer through vitamins, bile acids, SCFAs, and tryptophan metabolites. It highlights microbe-linked metabolites that either sensitize tumors to ferroptosis or block it, shaping therapy response and resistance.

This review explains how gut microbiota metabolites—SCFAs, bile acids, and tryptophan products—shape ferroptosis in intestinal epithelial cells and influence IBD severity, highlighting microbial patterns linked to lower butyrate producers and altered bile acid signaling.

This study shows that gut microbiota–derived short-chain fatty acids can reduce erastin-induced lipid peroxidation and modulate iron and ATF3 signaling in cardiomyocytes. The findings link microbial metabolites to ferroptosis control during ischemic-like stress in heart cells.

This review connects gut microbiota dysbiosis to ferroptosis biology in chronic kidney disease, emphasizing how microbial metabolites and altered antioxidant defenses can amplify iron-driven lipid peroxidation. It highlights functional shifts toward fewer SCFA producers and more uremic toxin producers and discusses diet and microbial interventions.

This review explains how ferroptosis drives tubular injury in acute kidney injury through iron overload and lipid peroxidation. It connects key regulators like system Xc−, GPX4, Nrf2, and ACSL4 to AKI models and highlights drug strategies that block ferroptosis.

This review explains how ferroptosis drives lipid peroxidation and brain injury in ischemic and hemorrhagic stroke. It summarizes drug targets and inhibitors such as ferrostatin-1, liproxstatin-1, selenium/GPX4 support, N-acetylcysteine, and iron chelation, and it discusses translation limits.

This study shows that GPX4 protects neurons by anchoring to membranes through a hydrophobic fin-loop. A patient R152H mutation collapses this loop, triggers ferroptosis in patient neurons and organoids, and drives Alzheimer’s-like brain signatures in mice.

This review connects Alzheimer’s neurodegeneration to ferroptosis, an iron-driven, lipid-peroxidation cell-death program. It summarizes human and model evidence linking brain iron, GPX4 antioxidant defense failure, and amyloid/tau-related iron handling to cognitive decline, and outlines therapy angles that target iron–redox stress.

This review links ferroptosis to Alzheimer’s and Parkinson’s disease by connecting iron imbalance, mitochondrial stress, and lipid peroxidation to neuronal loss. It highlights LOX-driven oxidized phospholipids, ACSL4-dependent lipid vulnerability, VDAC2-related iron handling, and ferritinophagy as key mechanisms, and it prioritizes Nrf2/Bach1 as actionable therapeutic targets.

This study shows that T-cell stimulation lowers GPX4 protection and shifts activated T cells toward ferroptosis. Ferroptosis vulnerability varies by subset and tracks with GPX4 expression. GPX4 inhibition weakens CAR-T killing and cytokine output, while ferroptosis inhibition restores function and improves antitumor activity.

This review explains how ferroptosis shapes tumor immunity. Tumor ferroptosis can boost antigen presentation and T-cell killing, but ferroptosis in immune cells weakens surveillance and therapy response. Key control points include GPX4, system Xc−, iron handling, and lipid peroxidation.

What was reviewed?This review explored the role of selenium in ferroptosis, focusing on its essential involvement through glutathione peroxidase 4 (GPX4), a key selenoenzyme that protects against lipid peroxidation and ferroptosis. It examines the dual role of selenium in regulating iron-dependent lipid peroxidation and the mechanisms through which selenium, via GPX4 and other selenoproteins, helps […]

This study demonstrates that GPX4 is essential for motor neuron survival, with its ablation in mice leading to rapid motor neuron degeneration and paralysis via ferroptosis. Vitamin E supplementation delays disease onset, highlighting the potential for ferroptosis inhibition in treating neurodegenerative diseases.

This study identifies GPX4 as essential for human erythroblast enucleation, independent of ferroptosis. The results show that lipid raft clustering and myosin phosphorylation, which are necessary for enucleation, are disrupted in GPX4-deficient cells, and cholesterol supplementation can partially restore enucleation efficiency.

What Was Studied?The research paper reviewed the roles of GPX4 (Glutathione Peroxidase 4) in cell death, particularly focusing on its function in ferroptosis, autophagy, and disease. GPX4, a key selenoenzyme, plays a pivotal role in mitigating lipid peroxidation, thus protecting cells from oxidative stress and various forms of regulated cell death (RCD). The study explores […]

This review explains why stopping membrane lipid peroxidation is the most reliable way to block ferroptosis. It compares endogenous defenses with synthetic inhibitors and shows that optimized radical-trapping antioxidants offer the strongest in vivo potential, while many upstream strategies remain less consistent across models.

This review explains how a gut bacterial tryptophan metabolite, IDA, can promote colorectal cancer by blocking ferroptosis through an AHR–ALDH1A3–FSP1–CoQ10 pathway. It reframes microbial metabolites as direct regulators of tumor cell death vulnerability, not just immune modifiers.

What was studied?This was an experimental mechanistic study that tested whether GPX4 is a central regulator of ferroptosis and whether chemically inducing GPX4 failure can selectively kill cancer cells and suppress tumor growth. The authors compared multiple ferroptosis-inducing small molecules and used metabolomics, chemoproteomics, and genetic modulation to map where these compounds converge. They showed […]

This review explains how ferroptosis, driven by iron dysregulation and lipid peroxidation, exacerbates neuronal injury in ischemic stroke. It evaluates therapeutic strategies like ferrostatin-1, liproxstatin-1, and iron chelation, highlighting FABP5 as a potential biomarker for monitoring ferroptosis in stroke.

This review explains how ferroptosis drives kidney injury through iron-dependent lipid peroxidation when GPX4- and FSP1-based defenses fail. It highlights proximal tubule vulnerability, links ferroptosis to ischemia–reperfusion and nephrotoxins, and summarizes anti-ferroptotic strategies that protect kidneys in models.

This review explains how lipid metabolism drives ferroptosis by shaping oxidation-prone membrane phospholipids and controlling iron-dependent lipid peroxidation. It highlights ACSL4 and LPCAT3 remodeling, GPX4 and system xc− defenses, and backup antioxidant pathways such as FSP1–CoQ10 and GCH1–BH4, with implications for cancer and tissue injury.

This review explains how ACSL enzymes reshape tumor fatty-acid use and control ferroptosis and cancer immunity. It contrasts ACSL4-driven polyunsaturated lipid remodeling that promotes ferroptosis with ACSL3-oleic acid programs that resist ferroptosis, and it links these pathways to immunotherapy response.

This review explains ferroptosis, an iron-driven, lipid peroxidation cell-death pathway linked to metabolism and redox balance. It highlights key control points such as system xc−, glutathione, GPX4, lipid remodeling, and iron handling, and it connects these mechanisms to cancer and tissue injury.

What was reviewed?This paper reviewed ferroptosis as a regulated, non-apoptotic form of cell death driven by iron-dependent lipid peroxidation, then mapped the main molecular “pressure points” that determine whether cells resist or enter ferroptosis. It focused on core chemistry (iron handling and lipid oxidation), the best-supported defense systems that stop membrane damage, and how organelles […]

What was studied?This study defined and experimentally mapped a distinct form of regulated cell death that the authors named ferroptosis. They used the RAS-selective small molecule erastin to trigger this phenotype, then tested what conditions were required for death, what cellular damage accumulated first, and how this process differed from apoptosis, necrosis, and autophagy. They […]

Ferroptosis links metabolism to disease because it depends on iron handling and membrane lipid chemistry. Tumors, neurodegeneration, and organ injury models often shift ferroptosis sensitivity by changing cystine uptake, glutathione levels, GPX4 activity, and alternative antioxidant pathways such as FSP1–CoQ10.

This study shows a selective small molecule can block colibactin production by inhibiting the activating enzyme ClbP. The inhibitor stops colibactin-linked DNA damage signals and DNA adduct formation in infected cells and remains effective in a fecal microbiome model without broad antibiotic effects.

This review explains how gut microbiota can guide cancer screening and treatment, focusing on colibactin-producing E. coli in colorectal cancer. It links pks-positive E. coli to DNA damage, mutational fingerprints, senescence, and immune changes, and it outlines ways to target colibactin activity.

This addendum explains how colibactin-producing E. coli can speed colon tumor growth by inducing senescence and a growth-factor secretory program. The pathway runs through c-Myc, miR-20a-5p, SENP1, and altered p53 SUMOylation, with HGF signaling driving proliferation of nearby uninfected tumor cells.

What was studied?This study performed a meta-analysis to clarify whether carrying colibactin-producing pks+ Escherichia coli associates with a higher risk of colorectal cancer (CRC), because prior individual studies reported conflicting results. The authors systematically searched major databases up to October 18, 2021, extracted case–control and cohort data where CRC status was confirmed and pks genes […]

his study shows colibactin-producing bacteria directly create DNA interstrand cross-links in human cells, triggering ATR replication stress and Fanconi repair responses. Blocking colibactin maturation or adding ClbS prevents cross-links, and inhibiting ATR or FANCD2 lowers cell survival, defining ICLs as the key lesion.

This study shows colibactin harms bacteria, triggers DNA damage defenses, and leaves a bacteria-specific mutation signature. Colibactin kills neighboring E. coli under contact-rich conditions, induces A/T-motif mutations (often T→A), and even causes self-damage in pks+ producers despite resistance.

What was studied?This study used structural biology to define how ClbK, a PKS–NRPS hybrid “megaenzyme” encoded by the pks biosynthetic gene cluster in colibactin-producing Enterobacteriaceae, is built and how its architecture could support a key elongation step in colibactin assembly. The authors focused on the complete trans-AT PKS module of ClbK and the full-length hybrid […]

This review explains how colibactin damages host DNA and also triggers bacterial SOS responses and prophage induction, reshaping gut communities and virulence. It connects barrier loss and inflammation to higher genotoxic risk and frames colibactin genes as functional microbiome biomarkers.

This mini-review explains how pks-positive E. coli make colibactin and how it drives colorectal cancer through DNA crosslinks, double-strand breaks, and mutational signatures such as SBS and ID-pks. It also summarizes key toxin-maturation steps that may enable targeted prevention.

This review explains how pks+ E. coli control colibactin production and why iron, oxygen, inflammation, diet, and drugs change DNA damage risk. It highlights ClbR regulation, inflammation-linked clb upregulation, and interventions such as mesalamine, d-serine, and SCFAs that can reduce genotoxicity.

This study found that many SPF laboratory rats carry phylogroup B2 E. coli with genotoxins, especially the pks colibactin island, and that vendor source strongly affects prevalence. These strains cause toxin-typical cytopathic effects and may confound rat models of infection, inflammation, and cancer.

This review explains how pks-positive bacteria produce colibactin, how it damages host DNA, and why it links to colorectal cancer and invasive infection severity. It also summarizes toxin-pathway inhibition as a prevention strategy while noting pks-derived anti-inflammatory and analgesic effects.

Colibactin is a microbiome-derived genotoxin produced by a subset of gut-associated bacteria that carry the pks (clb) biosynthetic gene cluster. Rather than acting like a classical acute toxin, colibactin is clinically relevant because it can chemically damage host DNA, creating lesions that are difficult to repair and that may leave persistent mutations if cells survive. In a microbiome systems context, colibactin is best understood as a functional output of specific bacterial metabolism that can intersect with host genome stability, particularly at the intestinal epithelial interface.

The human microbiome plays a critical role in metal metabolism, influencing both metal absorption and the potential for mismetallation in the body. Studies show that heavy metals can disrupt microbial diversity, leading to dysbiosis and altered metabolic functions in the gut. Moreover, some microbes possess the ability to sequester toxic metals, preventing their absorption and thus minimizing the risks of mismetallation in host tissues. As research in this area progresses, understanding these microbiota-metal interactions will be crucial for exploring new avenues in the prevention and treatment of metal-associated diseases.

What was reviewed?This review focuses on the role of probiotics, specifically lactobacilli, in bioremediation and the detoxification of heavy metals. The paper reviews how microbial processes, especially those of gastrointestinal bacteria, interact with heavy metals like arsenic, cadmium, mercury, and lead. It emphasizes the potential of probiotics in removing or sequestering these metals from the […]

This review examines how metal(loid) exposure affects gut microbiota composition and function. It also evaluates microbiota-related strategies for metal(loid) detoxification.

This study explores the essential role of metal ions in human health, detailing their involvement in enzyme catalysis and the impacts of imbalances on diseases. It also highlights potential clinical applications for metal-based therapies.

This review examines bacterial metallostasis, focusing on metal sensing, metalloproteome remodeling, and metal trafficking. It highlights key regulatory mechanisms and implications for therapeutic interventions and synthetic biology.

This review examines the role of metallochaperones in copper and nickel ion transport, highlighting their significance in metal ion homeostasis and implications for treating diseases like Wilson’s and Menkes diseases.

This review explores the biological roles of essential metals in human health, focusing on their contributions to enzymatic functions and redox reactions. It also highlights how dysregulation of metal homeostasis can lead to diseases like Alzheimer’s, Parkinson’s, and cancer.

This study explores how trace metals impact gut microbiota composition and pathogen competition, emphasizing nutritional immunity and the potential for probiotic interventions to enhance pathogen resistance.

This review examines the role of altered wild-type SOD1 in Parkinson’s disease, highlighting its involvement in dopamine neuron degeneration and presenting a novel mouse model for studying SOD1-related pathologies.

This review examines the role of lysosome-related organelles in regulating metal homeostasis, focusing on how these organelles store and transport metals like copper, zinc, and iron to maintain cellular balance and protect against toxicity.

The review examines how exposure to arsenic, cadmium, lead, mercury, and thallium impacts the cardiovascular system and oxidative mechanisms in children, highlighting long-term health risks and suggesting preventive strategies.

This review addresses the health effects, toxicity mechanisms, and therapeutic interventions related to heavy metals, highlighting the importance of further research and improved treatment strategies.

This study examines how cadmium exposure suppresses iron transport in the duodenum, leading to iron deficiency anemia. The research reveals the molecular mechanisms behind this disruption and its broader health implications.

This study investigates metallochaperones in plants, focusing on their role in metal homeostasis, detoxification, and stress responses. These proteins are essential for managing toxic metals like cadmium and enhancing plant resistance to environmental stressors and pathogens.

This study explores the role of metallochaperones in bacteria, focusing on how they deliver essential metal ions to metalloproteins and maintain metal homeostasis under metal stress. These mechanisms are vital for bacterial survival, especially during infection.

This study explores the effects of oxidative stress on metallation in E. coli enzymes, focusing on the competition between iron, zinc, and manganese for enzyme binding sites, and the protective role of manganese in restoring enzyme activity.

What was studied?The study investigates the metal preferences and metallation processes of enzymes, particularly focusing on the role of metal ions in metalloenzyme function. It explores how cells regulate the binding of metals to enzymes and how these metals impact enzymatic activity. The study also delves into the competitive nature of metal ions such as […]