Articles tagged with Transgenic Mice
Researchers have developed a dual-targeting strategy to combat emerging infectious diseases. A fully human monoclonal antibody cocktail provides complete protection against lethal Nipah virus infection, even when treatment is given after infection has begun.
Research links oral bacteria to Parkinson's disease via the gut-brain axis, finding Streptococcus mutans produces metabolite imidazole propionate that contributes to disease progression. Targeting the oral-gut microbiome may offer a new therapeutic approach for Parkinson's treatment.
Researchers have found that mice can instinctively exhibit rescue-like behavior toward anesthetized conspecifics without prior training or external rewards. Oxytocin neurons in the paraventricular nucleus are activated when detecting distress signals, releasing OXT and coordinating emotional and motor responses.
This study reveals NAT10 is crucial for spermatogonial proliferation and differentiation. In Nat10-deficient mice, infertility occurs with reduced testicular sizes, germ cell depletion, and a loss of spermatogonial homeostasis.
Researchers investigated why bones become less responsive to exercise with age, finding increased mtROS or decreased Atg7-dependent autophagy in osteoblastic cells do not contribute to reduced mechanoresponsiveness. Damage to the bone's osteocyte network also does not prevent a healthy bone-building response.
A USC Stem Cell mouse study has identified shared genes involved in regenerating cells in the ear and eye, which could lead to new treatments for hearing and vision loss. The researchers discovered that inhibiting a specific protein, p27Kip1, can encourage regeneration in both organs.
Researchers have identified a novel mechanism of intercellular communication involving mRNA transfer between different types of stem cells. This phenomenon enables cell fate conversion and reverts human pluripotent stem cells to an earlier embryonic stage.
The study highlights the role of the Nwd1 gene in liver disease and its potential as a therapeutic target. Mice with Nwd1 gene deletion exhibited liver pathologies mirroring MASH, including excessive lipid accumulation and increased ER stress.
Researchers discovered a novel mechanism of intercellular communication through mRNA transfer between stem cells, allowing for biologically significant effects such as cell fate conversion and pluripotent state maintenance.
Research identifies IL-1R1-expressing neurons in key brain regions, including the somatosensory cortex and hippocampus, which regulate sensory processing, mood regulation, and memory. The study provides new insights into how inflammation contributes to sensory, mood, and memory disorders.
Overexpressing hepatic SLC7A11 leads to glutamate and serine deficiency, promoting MASLD progression through ferroptosis. Serine supplementation rescues the disease phenotype.
Dr. Gail Cornwall is investigating the structure of the brain extracellular matrix, a network of proteins and polysaccharides found in the space between neurons and glia. Her research aims to identify novel structural elements and mechanisms that enable brain plasticity and sex-specific responses.
A new study found that heat therapy positively modulates multiple physiological parameters in APP/PS1 mice, with improved memory in males and worsening effects on females. This highlights the importance of personalized treatments based on sex-specific responses to therapy.
A new study detects pre-malignant pancreatic lesions using Diffusion Tensor Imaging (DTI), a form of MRI, which could enable early diagnosis and effective therapies. The detection was successful in both transgenic mice and human samples, opening the way to non-invasive diagnostic tools for PanINs.
A new study reveals that glyphosate exposure in mice can cause lasting brain inflammation and accelerate Alzheimer's disease-like pathology, even after a significant pause from exposure. The herbicide's byproducts have been found to accumulate in brain tissue, raising serious concerns about its safety for human populations.
Researchers from Indiana University have uncovered how the EphA2 protein receptor contributes to cataract formation. The study found that canonical ligand-dependent EphA2 signaling remains stable in aging lens tissue, while non-canonical signaling increases with age, affecting lens fiber cell maturation.
Researchers used a mouse model to assess the impact of senolytic agents dasatinib and quercetin on pelvic organ prolapse. The study found that D+Q injections did not result in significant differences in prolapse development but reduced cellular senescence markers.
Researchers at WVU are working on a project to inhibit the myeloperoxidase enzyme, which feeds pancreatic cancer growth. By targeting this enzyme, they hope to boost the body's immune system to fight cancer, showing promise in mouse models and potential for future clinical trials.
Researchers have developed a humanized mouse model with a fully functional human immune system, enabling the study of immunotherapy development, disease modeling, and vaccine development. The new model, called TruHuX, mounts specific antibody responses and can develop full-fledged systemic lupus autoimmunity.
Scientists have discovered that ADGRF5 helps maintain the integrity of the glomerular filtration barrier, which is critical for filtering waste from the blood. The study found that disrupting ADGRF5 expression led to abnormalities in the glomerular basement membrane and increased albuminuria.
Researchers at OIST have discovered a novel treatment that effectively reverses the symptoms of Alzheimer's disease in mice. The treatment, PHDP5, targets the dynamin-microtubule interaction and restores communication between neurons inside synapses.
Researchers at Johns Hopkins Medicine used genetically engineered mice to study the mechanism of congenital stationary night blindness. The findings demonstrate that a mutation in the rhodopsin gene produces unusual background electrical activity, desensitizing rods and causing poor vision in low-light settings.
Researchers at RIKEN Center for Brain Science discovered neural circuitry in the spinal cord that enables brain-independent motor learning and recall. The study found two critical groups of neurons: one necessary for new adaptive learning and another for recalling adaptations once learned.
A study published in Brain, Behavior, and Immunity found that normal levels of interferon-β are required for normal memory function, and its absence changes nerve cell components in a sex-dependent fashion. The research also showed that higher or lower than normal levels of interferon-β affect the brain in a sex-dependent manner.
Researchers used single-cell RNA sequencing to analyze the effects of APC treatment on AD transgenic mice, revealing alterations in glial cells and upregulated genes associated with AD progression. APC treatment downregulates inflammatory processes and recovers nervous system functions.
Researchers found GV1001 decreases BACE and Aβ1-42 levels, reducing neurodegeneration and senescence in 3xTg-AD mice. It also increases survival, telomere length, and telomerase activity, contributing to improved lifespan.
A recent study has uncovered 145 genes crucial for genome stability, shedding light on genetic factors influencing human health over a lifespan. The research highlights the potential of SIRT inhibitors as a therapeutic pathway for cohesinopathies and other genomic disorders.
Researchers from Florida Atlantic University found that alpha-santalol, a compound in sandalwood oil, decreases cell proliferation and induces apoptosis to prevent prostate cancer development. The study showed a 53% increase in normal tissue area in treated mice, indicating protection against prostate cancer progression.
Researchers discovered that microRNA-29 can restore normal skin structure rather than producing a scar, promoting faster and more efficient wound healing. The release of microRNA-29 targets, particularly LAMC2, is crucial in this process, suggesting a potential new approach for treating large-area or deep wounds.
A team of neuroscientists has discovered that oligodendrocytes, myelin-forming cells, accelerate glucose consumption to deliver energy-rich molecules to rapidly firing axons. This communication is mediated by potassium signals and maintains axonal health.
A Cornell University study using lab mice with human genes found that male mice exposed to arsenic developed insulin resistance and Type 2 diabetes, while female mice did not. The researchers identified a biomarker called miR-34a associated with insulin resistance in Type 2 diabetes.
Researchers found that mutations in IDO2 can affect dopamine release and lead to ASD-like behaviors. IDO2 KO mice exhibited changes in microglia populations, which may contribute to synaptic abnormalities.
Researchers discovered that RvD2, a specialized proresolving lipid mediator, can alleviate established liver scarring or fibrosis. Treatment with RvD2 improved liver histopathology and increased bone marrow and blood monocytes.
The Cre-LoxP system's specificity is compromised due to non-specific promoters driving Cre expression, leading to inaccurate results. This limitation requires careful consideration for proper interpretation of experimental outcomes.
Researchers characterized changes in cognitive behaviors, neuronal morphology and gene expression in a tauopathy mouse model. The study found significant decreases in dendritic arborization and synaptic gene upregulation over time.
A new neural circuit has been discovered in the brain that produces a strong sense of discomfort when activated. The study found that the subthalamic nucleus, which controls voluntary movements, also plays a role in the development of depression.
Researchers at the University of Texas Health Science Center discovered a gene therapy approach that can restore motor functions in mice with Contactin-Associated Protein 1 (Cntnap1) mutations. The study found that turning on the normal gene earlier improves the rescue outcome, and the next phase is to test this approach in humans.
Sahmyook University researchers discovered a correlation between methamphetamine-induced behavior and the expression of specific genes in mice models lacking Period 2 gene. They identified 19 genes that were activated only in response to repeated doses of methamphetamine.
Researchers identified a new class of molecules capable of preventing excessive inflammation in severe COVID-19. Blocking the link between peptide C5a and its cellular receptor reduced lung damage and other complications in mice. This finding suggests that antagonists of C5aR1 could be useful for treating severe COVID-19.
A study published in Nature Communications reveals a small secreted protein NICOL regulates lumicrine-mediated sperm maturation and male fertility. The research team discovered that mice lacking NICOL were sterile, indicating its importance for the sperm-maturation pathway.
Researchers found that p21 knockout mice experienced reduced senescent cell presence, alleviated chronic lung inflammation, and improved fitness. Resident epithelial and endothelial cells played a significant role in mediating the p21-dependent inflammatory response.
A team of researchers from Ohio University discovered that CIDEC protein improves vascular and metabolic dysfunction, reducing insulin resistance and lipid levels in high-fat diet-induced mice. The study contributes to understanding the role of the vascular endothelium in regulating systemic metabolism.
Researchers developed a VR imaging system to measure neural activity in mouse brains during behavior, revealing abnormalities in cortical functional network dynamics associated with autism. The system successfully distinguished between autism model mice and wild-type mice based on their brain network patterns.
Researchers found that suppressing AMPKα1 but not AMPKα2 isoforms improved aging-related impairments in mice. The study revealed novel insights into the roles of AMPK signaling pathway in cognitive aging.
Researchers found that platelet depletion increased amyloid plaque size and neuronal damage in APP-PS1 mice. However, platelets may have a beneficial role in limiting plaque growth and attenuating neuritic dystrophy at advanced stages of Alzheimer's disease.
Researchers found that clearance of p16Ink4a-positive cells did not impact β-cell mass, but improved β-cell function and proliferative capacity in a subset of HFD mice. The targeted subpopulation of β-cells is non-proliferative and non-SASP producing.
A recent study found that the APOBEC3G enzyme can cause numerous mutations in bladder tumor cells, leading to increased malignancy and mortality. The research suggests that this enzyme could be a potential target for cancer treatment strategies.
Researchers discovered that eliminating a serotonin receptor enhances fear extinction, leading to improved therapy outcomes for PTSD patients. This finding may help develop targeted treatment strategies by understanding the role of SSRIs in modulating brain activity.
A new gene therapy approach has been developed to boost the expression of the beta-3 adrenergic receptor in heart cells, improving mitochondrial function and preventing or reversing heart failure in a mouse model of aortic stenosis. This could potentially provide new therapeutic options for patients with this condition.
Scientists at the University of Tsukuba have identified a system to transport excess reactive sulfur species out of cells, maintaining redox homeostasis and preventing oxidative stress. This discovery opens new avenues for research into sulfur stress and related diseases.
Researchers created genetically edited mice to label and study secretome proteins, facilitating studies of inter-organ communication. The transgenic mice enable scientists to identify specific cell types and organs, providing a valuable resource for mapping and profiling the secretome.
A new gene therapy approach using the neuroprotective protein SynCav1 has shown promising results in slowing down ALS disease progression and increasing life span in rodent models. The treatment preserved spinal cord motor neurons and extended longevity in mice, with similar effects observed in a rat model of ALS.
A new study found that HIV-1 Tat expression accelerates age-related diseases in male mice by disrupting neuroendocrine function. Researchers discovered that Tat alters steroid hormone levels, leading to anxiety-like behavior, cognitive errors, and reduced grip strength.
A study by UC Riverside researchers shows that reactivating the Fmr1 gene in young transgenic mice with Fragile X syndrome eliminates symptoms. This breakthrough treatment offers hope for young children living with FXS and suggests targeting early brain development may be effective.
Researchers designed and tested 32 inhibitors targeting the SARS-CoV-2 main protease, a key viral protein required for replication. The study found six compounds with high potency to protect cells from infection, offering promise for the development of orally available anti-SARS-CoV-2 drugs.
Researchers discovered that DAPPD promotes phagocytosis of microglia cells, leading to reduced amyloid deposition and improved cognitive function. The study suggests that targeting neuroinflammation may be a viable therapeutic strategy for neurodegenerative diseases.
A new vaccine candidate has been developed to treat and prevent toxic shock caused by invasive streptococcal disease. The 'J8' vaccine candidate has shown a 1000-1,000,000 fold reduction of bacterial burden in treated mice.
Scientists at Hong Kong University of Science and Technology discover that interleukin-33 (IL-33) rescues contextual memory deficits and reduces beta-amyloid peptide deposition in AD mouse models, suggesting a new therapeutic intervention.
A study by Université Laval researchers found that a drop in body temperature associated with aging can aggravate the main manifestations of Alzheimer's disease. The study used transgenic mice to demonstrate this link and suggests that thermoregulation therapy could be a potential treatment option.
Researchers found that anti-dsDNA, surface-expressed TLR4, and endosomal TLR9 cooperate to worsen lupus progression. Co-activation of these receptors triggers a more intense immune response, leading to increased disease severity.