The Growth Arrest and DNA Damage-Inducible 45 (GADD45) proteins, including GADD45α, GADD45β, and GADD45γ, play a crucial role in the cellular stress response and maintaining genome stability. These proteins are involved in various biological processes, including cell cycle arrest, DNA repair, apoptosis, and senescence, particularly when cells encounter genotoxic stress.

Autophagy, from Greek , meaning and , is a highly conserved cellular pathway responsible for the degradation and recycling of long-lived proteins. A functional autophagy pathway, characterized by cell- and tissue-specific basal autophagy activity, is crucial for the cell's successful response to aging and the mitigation of age-related pathologies. However, comprehensive understanding of underlying mechanisms and spatiotemporal profiling of autophagy flux across tissues remain largely elusive.

Epilepsy often presents numerous comorbidities, including anxiety, depression, and cognitive deficits. Epilepsy is not only restricted to GABA/glutamate imbalance, as researchers are delving more into finding the possible causal inference between other factors; one such recognized interplay is between seizures, stress, and inflammation. Stress-induced hypothalamic-pituitary-adrenal (HPA) axis activation increases corticosteroid release, which binds to mineralocorticoid receptors (MR), intensifies the release of neuroinflammatory markers, lowers seizure threshold, and worsens seizure susceptibility.

Cyclin-dependent kinase 7 (CDK7) is a key regulator of transcription and the cell cycle, with its dysregulation linked to tumorigenesis and chemoresistance. CDK7 serves as an unfavorable prognostic marker in multiple cancers and is significantly overexpressed in patients with poor prognosis, including those with lung and pancreatic cancer.

Recent advances in cancer immunotherapy have improved patient outcomes, even in advanced stages of the disease. However, the effectiveness of current cancer immunotherapies remains limited to a small subset of patients because of resistance and an immunosuppressive tumor microenvironment.

With the increasing prevalence of aging populations, the incidence of neurodegenerative diseases continues to rise, posing a serious threat to human health and quality of life. Owing to the highly complex pathogenesis of these disorders, the identification of effective therapeutic targets remains a major challenge. CD44, a cell surface glycoprotein, plays a central role in regulating cell proliferation, survival, adhesion, and migration. Emerging evidence further indicates that CD44 contributes to NF-κB activation, thereby amplifying inflammatory responses.

Proteases are essential enzymes that regulate protein turnover and activate signaling pathways through targeted peptide bond cleavage. While traditionally regarded as degradative agents, proteases are now recognized for their diverse roles in health and disease, particularly in cancer and viral infections. Advances in high-throughput, mass spectrometry-based technologies have enabled proteome-wide identification of protease substrates, revealing numerous potential therapeutic targets. As large-scale approaches yield expansive substrate lists, it is increasingly important to understand the roles of disease-related proteases within their specific biological contexts.

Attention-deficit/hyperactivity disorder (ADHD) is a common neuropsychiatric disorder of inattention, hyperactivity, and impulsivity. Roles for dopamine and norepinephrine are widely recognized; however, the role of serotonergic neurotransmission is less clear. This systematic literature review aimed to determine if changes in serotonin transmission are implicated in the neurobiology of ADHD.

Epilepsy is a chronic neurological disorder leading to repeateduncontrollable seizures. The available armamentarium of ~ 30 antiseizure drugsis unable to control seizures in a third of the patients, which signifies the need to look for novel therapeutic targets with alternative mechanisms of action.

Hypertension is a major health problem worldwide, yet fewer than half of patients maintain adequate blood-pressure control, pointing to hidden pathogenic drivers and therapeutic gaps. Normal pressure regulation depends on seamless cross-talk among the kidney, vasculature, brain, and gut; once this dialogue falters, low-grade, T cell-centered inflammation sustains disease.

The most prevalent solid cancer in young adult males is testicular germ cell tumors (TGCTs), which are becoming more and more common globally. Approximately 20% of patients with metastatic disease relapse or develop resistance to cisplatin-based chemotherapy, despite its high effectiveness, underscoring the need for alternative therapies.

Rhabdomyosarcoma (RMS), predominantly diagnosed in children, represents 3% of the pediatric solid tumors. RMS has characteristics of skeletal muscle, although the cell of origin remains controversial. Cytotoxic therapeutics, radiation treatment and surgery remain the standard of care; however, outcomes for advanced disease have not changed for several decades. Major research advances over the past two decades have defined molecular subtypes and driver mutations that could provide new therapeutic targets.