281 papers
Molecular biology explores the tiny machinery inside living cells, revealing how genetic instructions are read, copied, and turned into the proteins that keep us alive. This field acts as a bridge between the static code of DNA and the dynamic processes that drive growth, disease, and life itself, offering insights into everything from cellular repair to the development of new medicines.
On Gist.Science, we track every new preprint uploaded to bioRxiv in this category to make these complex discoveries accessible to everyone. Our team processes each submission to provide both clear, plain-language explanations and detailed technical summaries, ensuring you can grasp the core findings without getting lost in dense academic jargon.
Below are the latest molecular biology papers freshly processed from bioRxiv, ready for you to explore and understand.
This study demonstrates that repurposed small-molecule inhibitors targeting metalloproteinases and phospholipases effectively neutralize a diverse range of venoms from the Neotropical *Bothrops* snake genus, suggesting their potential as valuable early interventions for snakebite treatment.
This study utilizes ITS2, COI, and COII molecular markers to reveal that the *Anopheles tessellatus* complex in Indonesia comprises three distinct genetic lineages across five islands with high haplotype diversity and potential speciation in specific populations, highlighting the need for further research to clarify its role in malaria transmission.
This study reveals that the performance of destabilized fluorescent reporters in *C. elegans* is critically dependent on the specific combination of fluorophore and epitope tag, demonstrating that certain configurations (such as a 3xFLAG adjacent to a PEST sequence or the use of mStayGold) can severely compromise the ability to detect dynamic gene expression oscillations.
This study presents RAStoERK, a comprehensive reference interaction atlas that maps the interactomes of the RAS/RAF/MEK/ERK pathway components and their mutations to reveal paralog-specific roles, mutation-driven rewiring, and novel crosstalk with processes like mRNA metabolism and WNT signaling, thereby providing a foundational resource for understanding the pathway's integration into physiology and disease.
This study investigates the limitations of quantitative DNA metabarcoding by demonstrating that high variation in mitochondrial copy numbers and stable PCR amplification biases prevent accurate biomass estimation, ultimately revealing fundamental constraints and the need for new methodological approaches despite the development of a mathematical model to correct for these biases.
This study demonstrates that in metabolomic analyses of small organisms, both pool size and biological replication are critical, interdependent factors that jointly determine the detectability and stability of biological signals, where insufficient pooling or replication leads to a loss of true metabolic effects without increasing false discoveries.
MuteFree is a novel AAV transfer plasmid system that eliminates ITR mutations through combinatorial optimization of the plasmid backbone and flanking sequences, thereby enabling high-fidelity, high-yield production of therapeutic AAV vectors compatible with GMP manufacturing.
This study demonstrates that in budding yeast, constitutive AMPK activity decoupled from fatty acid synthesis inhibition prevents senescence and preserves late-life fitness in all aging cells by resolving the metabolic conflict between mitochondrial Acetyl-CoA transport and lipid starvation.
This study demonstrates that clindamycin resistance in *Plasmodium falciparum* arises from mutations in apicoplast 23S rRNA genes, which, despite potentially impairing in vitro growth, do not completely block the parasite's ability to infect mosquitoes and spread in the field.
This study demonstrates that while the eIF4G-PABP closed-loop architecture is dispensable for productive translation initiation, it can be actively co-opted through specific proteolytic cleavage to form a dead-end complex that potently represses translation, thereby explaining the distinct translational outcomes of factor depletion versus viral cleavage.