The new CRISPR 3.0 system allows for simultaneous activation of up to seven genes at once, demonstrating high accuracy and efficiency. This multiplexed gene activation system has significant potential for crop breeding and enhancement, enabling the discovery and translational science in plants.
Researchers from Kanazawa University found that gasdermin D forms pores in the cell membrane, allowing factors to flow in and activating IL-1® maturation. This study provides insight into the essential functions of the human immune system and the regulation of immune function.
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Researchers at Nagoya University identified a key enzyme that activates nitrate uptake mechanisms in plants responding to nitrogen starvation. The CEPH protein plays a critical role in activating the high-affinity transport system, which enables rapid nitrate uptake from the environment.
Researchers have identified the activation mechanism of SHP2, a key player in cancer development. The study reveals that flexible beta sheets, not previously thought to be crucial, open in the presence of a peptide, triggering SHP2 activation.
A recent study published in Cell Reports reveals that DNA supercoiling is involved in regulating gene expression, rather than being just collateral damage. The researchers found that specific genes are massively activated in response to stimuli, and topoisomerase TOP2A plays a crucial role in this process.
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A team of researchers at Tokyo Institute of Technology has identified a critical protein segment responsible for activating the MRN complex, a key player in DNA repair. The discovery reveals a conserved function across species, with implications for genetic disorders and gene editing applications.
Researchers at Ruhr-University Bochum have developed a method to control the direction of nerve fiber growth using magnetic nanoparticles. The team successfully implanted functionalized nanoparticles into model neurons, allowing them to guide axon growth and potentially promote regeneration in Parkinson's patients.
Researchers at University of Texas M. D. Anderson Cancer Center discovered NIK protein essential for T cell metabolic shift during activation, regulating anti-tumor immunity. Elevated NIK activity in T cells may improve adoptive therapy efficacy.
Researchers identified two inflammatory pathways involving complement and the inflammasome that promote abnormal blood vessel formation in wet AMD. Blocking these pathways, including essential proteins of the inflammasome, may lead to improved therapies for this common blinding disease.
Researchers at the Buck Institute have identified chronic inflammation as a driver of NAD+ decline, a key metabolite central to an efficient and healthy metabolism. Senescent cells activate CD38, which degrades NAD+, leading to age-related diseases. Blocking CD38 activity may offer a new target for therapeutic interventions.
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A new study found that coronaviruses use mimicry to trick human immune proteins, including those controlling blood coagulation and complement activation, which may drive pathology in infected patients. The researchers discovered over 150 protein mimics used by coronaviruses, including many involved in severe COVID-19 disease.
Biologists developed fluorescent mice to visualize protein kinase A (PKA) activation in the retina. They found that light stimulation activates PKA for nearly 15 minutes in rod cells, which are essential for night vision.
Researchers analyzed 113 patients' immune responses to COVID-19, identifying common patterns that predict severe outcomes. High levels of alpha interferon and inflammasome activation were linked to poor outcomes.
Acalabrutinib improved oxygenation levels and decreased molecular markers of inflammation in most patients with severe COVID-19. The treatment showed promise in reducing the severity of the disease, particularly among those on mechanical ventilation.
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Researchers discovered that helper proteins Swi5-Sfr1 and Rad51-related helpers collaborate to activate Rad51 in DNA repair. Mutations in Swi5-Sfr1 compromised activation, but yeast cells lacking Rad51-related helpers still repaired DNA, suggesting a compensatory role.
A recent study published in Science Advances found that physical forces alone can activate genes in human cells, leading to increased gene expression. The researchers discovered that histone proteins play a key role in determining which genes are responsive to stretching forces.
Researchers at MIT discovered that the waves produced on an egg's surface during fertilization are similar to those found in ocean and atmospheric circulations, as well as quantum fluids. The study reveals a universal wave pattern that helps organize cell division and formation of an organism.
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A new study led by the University of Pennsylvania School of Medicine reveals that the pioneering protein FoxA2 simultaneously binds to chromosomal proteins and DNA, opening gates for gene activation. This discovery helps untangle mysteries of embryonic stem cell development into organs, moving regenerative medicine forward.
Researchers discovered autophagy's selective degradation of protein liquid droplets but poor performance with aggregated proteins. This study used yeast and a test tube system to reconstitute the Ape1 isolation process, revealing the role of Atg8 and receptor proteins.
Researchers at the University of Zurich have identified a new target for treating incurable leukemia in children by analyzing the molecular causes of the disease. They found that an abnormal protein activates genes at the wrong time, triggering the formation of malignant white blood cells and causing leukemia.
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Researchers identify protein CaVbeta1E that promotes muscle mass maintenance via GDF5 signaling, counteracting sarcopenia. The study opens a new field of activity in developing therapeutic strategies against muscular decline associated with aging.
Researchers at Washington State University have identified a new therapeutic target for the treatment of gout, a common type of arthritis that causes episodes of painful and stiff joints. Blocking the signaling molecule TAK1 can suppress inflammation caused by gout, according to the study.
A research team at the University of Colorado School of Medicine has identified BRD4 as a central regulator of cardiac fibroblast activation. Chemical inhibitors of BRD4 potently block cardiac fibroblast activation, providing a potential therapeutic target for heart failure treatment.
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Researchers create a novel method using magnetic tweezers to study the mechanical forces that activate proteins like VWF, which initiates blood clots. The technique reveals the unfolding of VWF dimers under low forces, shedding light on the first step in blood coagulation.
LMU biologists have identified a general alarm signal that activates the Unfolded Protein Response (UPR) in mitochondria, ensuring protein degradation and restoring normal cell function. The signaling pathway is triggered by a decline in mitochondrial membrane potential and involves transcription factor ATFS-1.
A new strategy for designing light-sensitive proteins has been developed by researchers at Ruhr-Universität Bochum. They combined computer-aided and experimental methods to create a more targeted approach, enabling the manipulation of protein building blocks without impairing function.
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Researchers discovered two proteins that act like a 'clutch' in cells to activate the immune response. These protein condensates guide the movement of contents inside cells, much like switching gears in a car. The study sheds light on control mechanisms for immune activation and could lead to designing T cells with specific functions.
Researchers discovered two adaptor proteins that act as a 'clutch' to activate the immune response by moving protein condensates towards the center of cells. This discovery sheds light on the control mechanisms for immune response activation and could lead to designing immune cells to combat specific problems.
Researchers found that methylmercury increases cardiac fragility by removing an inhibitory brake on Drp1, a protein involved in mitochondrial fission. Treatment with a polysulfide group-releasing compound reversed this effect, suggesting a possible strategy to mitigate cardiotoxicity.
Yale scientists identify two proteins P300 and Brd4 as essential for activating the zebrafish genome after fertilization, allowing embryonic development to proceed. The discovery provides new insights into how life begins at a molecular level.
A study has revealed the structure of FoxM1 protein in its inactive state, which could lead to the development of new cancer treatments by stabilizing the protein. This understanding also provides insight into how transcription factors function and switch between active and inactive states.
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Scientists have discovered a previously unknown mechanism by which cells sense proteasome dysfunction and respond by editing the amino acid sequence of a key sensing protein. This finding has important applications for treating cancer, aging, and neurodegenerative diseases.
A team of biologists has discovered new rules governing cell decision-making in genetics, revealing how genes are activated under specific conditions. The study found that a protein called Zelda strengthens Dorsal activity, allowing cells to make decisions about gene activation based on their environment.
A new study reveals that BAX, a crucial driver of apoptosis, is activated by transient interactions with BH3-only proteins at two distant sites on the protein. This 'hit-and-run' interaction initiates the conversion of BAX into a lethal protein for cells.
A study published in Science Signaling reveals that the coralberry plant extract FR900359 can slow down aggressive uveal melanoma by targeting and inhibiting activated Gq proteins. The substance effectively stops cell division activity and suppresses cancer cell proliferation.
Researchers have developed a new live-imaging technique that detects short-lived leaks in epithelial tissues and reveals an active repair mechanism involving the protein Rho. This discovery could provide insights into diseases targeting the epithelial barrier, such as those caused by microbes, allergens, and cancers.
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Researchers at The Wistar Institute found that the S100A14 protein is expressed at higher levels in these individuals than control donors, activating natural killer cells to defend against HIV. This discovery may lead to novel approaches for prevention of HIV infection by manipulating host immune defense.
Researchers at Scripps Research Institute have discovered the molecular mechanisms of protein talin's activation of integrin on the cell membrane. This process is essential for cell adhesion and plays a crucial role in cancer progression and metastasis.
Scientists will investigate necroptosis, a form of programmed cell death, as a key contributor to neuronal loss in Alzheimer's. The goal is to develop therapeutics capable of blocking the necroptosis pathway and slowing or arresting cell death characteristic of the disease.
Medical researchers from MSU propose a new targeted cancer therapy by increasing the activity of wild-type p53, which supports genetic stability and prevents malignant tumor formation. The study reveals that p53 also regulates metastasis formation through various programmed cell death pathways.
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Researchers have identified P38 alpha as a crucial protein in activating brown fat cells to burn excess fat and eliminate the risk of obesity and related diseases. The study found that mice genetically modified to lack P38 alpha were protected against obesity, diabetes, and fatty liver disease.
Researchers at Kyoto University have discovered that MTSS1 controls the branching of neurons by activating one pathway and inhibiting another. This protein plays a dual role, regulating actin filaments to facilitate efficient and uniform coverage of the surrounding environment.
Researchers link abnormal TOR activity to oxidative stress and degeneration in both muscle cells and neurons. This discovery has broad implications for understanding diseases such as Alzheimer's, cancer, and HSP, and may lead to new therapeutic targets.
Researchers at Texas Tech University Health Sciences Center identified a specific amino acid residue responsible for inverting potassium channel communication. The study paves the way for developing novel and safer therapeutic drugs to correct illnesses associated with potassium channel dysfunction.
Research reveals that E. coli infection can induce delirium in aging rats by reducing levels of brain-derived neurotrophic factor (BDNF), a protein essential for long-term memory formation. The study suggests that immune system activation, such as after surgery or infection, may contribute to cognitive decline in the elderly.
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The researchers have identified a gene called Ankrd16 that prevents the production of harmful protein aggregates in neurological disorders such as Alzheimer's and Parkinson's disease. Elevating levels of Ankrd16 protects specific neurons from dying, while removing it leads to widespread buildup of abnormal proteins.
Cadm1 protein interacts with Kaposi's sarcoma viral proteins to promote inflammation and cancer growth in KSHV-infected cells. This discovery could lead to a new therapy targeting human protein CADM1 in viral-mediated cancers.
Researchers at Stanford University School of Medicine have found that young neural stem cells store large protein aggregates in lysosomes. Clearing these aggregates rejuvenates the cells' ability to activate and makes new neurons. The study highlights the importance of maintaining precise control over protein production and disposal.
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Researchers studying a rare skin disorder called DEB found that loss of collagen VII affected the cellular microenvironment, leading to abnormal mRNA and protein turnover. Meanwhile, another study used novel proteomics to characterize changes in O-GlcNAc modification sites on proteins involved in T cell activation.
Researchers provide foundational understanding of myostatin activation mechanism, shedding light on tolloid enzyme's role in generating active myostatin. The study's findings hold promise for developing novel therapies targeting specific structural states of myostatin.
The structure of chloride channel TMEM16A has been determined, revealing a unique activation mechanism that could restore hydration of the mucus layer in cystic fibrosis patients. Researchers believe that activating this channel could compensate for the defect in chloride ion secretion, paving the way for novel therapies.
A computer model developed by InSysBio scientists suggests that activating beta-amyloid degradation is key to preventing protein plaques in the brain. The model found that starting treatment at age 60 can lead to relative normalization of indices, highlighting the importance of early intervention.
Researchers have discovered that membrane lipids can activate the unfolded protein response (UPR), leading to increased protein production but also heightened sensitivity in cells. This new understanding may provide insights into various diseases, including those caused by viral infections and tumor growth.
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Researchers have discovered how Rice Stripe Virus (RSV) reproduces in small brown planthoppers, a key step in controlling the spread of devastating crop diseases. By studying interactions between proteins and compounds, they found that RSV activates the JNK signaling pathway to promote replication.
A University of Pennsylvania study found that social isolation in fruit flies leads to sleep loss, which causes cellular stress and activates the unfolded protein response (UPR). Chronic activation of UPR is linked to aging and age-related diseases such as Alzheimer's and diabetes.
Researchers find that members of the DUX family of proteins, specifically DUX4, trigger gene expression program in human embryos. DUX4 stimulates expression of genes induced during zygotic genome activation by binding to their regulatory regions.
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A recent study published in eLife provides a deeper understanding of p38α's structure and activation mechanism. The research reveals novel conformations that could be used to uncover new inhibitors, as well as important electrostatic interactions that may allow for alternative activation pathways with increased specificity.
Researchers discovered a protein signature that predicts leukemia, which could lead to novel treatments. The activation of STAT5 causes competition among proteins, leading to acute lymphoblastic leukemia.
Researchers discovered molecular mechanisms of how post-translational protein modifications influence apoptosis, a process of programmed cell death. This process is crucial for maintaining tissue homeostasis and preventing diseases such as Alzheimer's and Parkinson's.
A team of scientists has redefined the activation mechanism of the complement protein C1, a crucial part of the innate immune system. The study reveals that C1 is activated when two proteins are in close proximity, contradicting previous theories.