Ask about this productRelated genes to: SOS1 antibody
- Gene:
- SOS1 NIH gene
- Name:
- SOS Ras/Rac guanine nucleotide exchange factor 1
- Previous symbol:
- GINGF
- Synonyms:
- HGF, GF1
- Chromosome:
- 2p22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-10-27
- Date modifiied:
- 2019-04-23
Related products to: SOS1 antibody
Related articles to: SOS1 antibody
- Kirsten rat sarcoma viral oncogene homolog ()-G12D is a common oncogenic mutation in non-small cell lung cancer (NSCLC) and has posed significant challenges in the development of treatment approaches that specifically target this alteration. -G12D differs from -G12C in its biochemical and signal transduction features, which limits the use of drugs targeting the -G12C mutation, creating substantial demands in clinical contexts. This review sought to summarize the major developments in treatment for -G12D-mutant NSCLC, with a focus on the recent key advances and emerging clinical data on targeted therapies. - Source: PubMed
Publication date: 2026/07/20
Chen YihanChen MeilingXia YixinChen Jinliang - KRAS G12C has emerged as a clinically important therapeutic target in non-small cell lung cancer (NSCLC), representing a major advance in the treatment of KRAS-driven malignancies. The development of covalent inhibitors targeting the switch-Ⅱ pocket of inactive, GDP-bound KRAS has transformed a previously undruggable oncogene into a molecularly actionable target. First-generation KRAS G12C inhibitors, including sotorasib and adagrasib, have demonstrated clinically meaningful activity in previously treated NSCLC; however, their benefit is limited by acquired resistance, which arises through secondary KRAS alterations, bypass pathway activation, and adaptive reactivation of downstream MAPK signaling. In addition, treatment-related hepatotoxicity, particularly in the setting of prior or closely sequenced immune checkpoint inhibitor exposure, has emerged as an important clinical concern. Multiple next-generation KRAS G12C inhibitors, such as divarasib, glecirasib, and olomorasib, are currently under clinical development, with early evidence suggesting improved potency, selectivity, and tolerability. Furthermore, combination strategies incorporating immune checkpoint inhibitors and upstream or downstream pathway-targeted agents, including SHP2, SOS1, and MEK inhibitors, are being actively investigated to enhance the depth and durability of response. More recently, the advent of RAS (ON) inhibitors, exemplified by daraxonrasib (RMC-6236), has introduced a distinct therapeutic paradigm by directly targeting active RAS through a tri-complex mechanism. As the therapeutic landscape continues to evolve, optimal treatment selection will require integrated consideration of molecular heterogeneity, resistance mechanisms, toxicity profiles, and patient-centered shared decision-making. - Source: PubMed
Nakamichi ShinjiKubota Kaoru - The immune checkpoint receptor T cell immunoreceptor with Ig and ITIM domains (TIGIT) can signal via cytoplasmic motifs to regulate T cell function. The signaling molecules that mediate inhibitory TIGIT signaling and its regulation in T cells remain poorly defined. Here, proximity proteomics is employed to define TIGIT-proximal proteins upon CD155 engagement, identifying several that are ligation-specific, including those involved in signaling (Grb2 and SOS1), cytoskeletal regulation (CD2AP and SdcBP), and endocytosis (IST1 and SNX3). Through crosslinking followed by immunoprecipitation, we show that TIGIT and CD2AP directly interact, representing a novel association. A TIGIT mutant (Y225A/Y231A) incapable of inhibitory signaling prevents recruitment of these proteins. Strikingly, T cell receptor (TCR) stimulation is essential for TIGIT to engage with these pathways. Mechanistically, phosphorylation of TIGIT requires both CD155 ligation and TCR activation, resulting in its signaling and internalization. TCR activation-dependent TIGIT signaling establishes a regulatory mechanism that limits checkpoint control to when functionally required. - Source: PubMed
Publication date: 2026/08/05
Zammit William HLe Maistre Lucy JElliot Thomas A ECain Stuart AHumphries Martin JDavis Daniel MWorboys Jonathan D - Marine heatwaves pose significant threats to seagrass ecosystems, particularly during early life stages where recruitment governs population stability. In this study, we investigated propagule quality and stress tolerance mechanisms in the tropical seagrass Halophila ovalis by integrating density-based seed selection, antimicrobial storage, thermal priming and gene expression analysis. Density-gradient fractionation revealed clear stratification of seed quality, with high-specific-gravity seeds (SG > 1.20) exhibiting 78% germination compared to <12% in low-density fractions, indicating strong variation in physiological integrity. Storage experiments demonstrated that silver nanoparticle treatment (2 ppm AgNP) effectively preserved seed viability for up to 6 months, whereas copper treatments showed comparatively lower efficiency. Seedlings derived from high-density seeds were subjected to thermal priming (36 °C/40 psu) prior to exposure to extreme stress (41 °C/42 psu). Progressive 5-day priming significantly enhanced stress tolerance, with seedlings maintaining high survival (∼93%), shoot growth and photosynthetic area comparable to controls, while non-primed seedlings exhibited ∼31% mortality and ∼30% tissue loss. Biochemical responses indicated ∼60% lower lipid peroxidation (MDA) in primed seedlings, accompanied by elevated antioxidant capacity. At the molecular level, priming induced strong upregulation of stress-responsive genes, including HSPA1 (∼22-fold), SOD3 (∼21-fold) and osmoregulatory genes (VP1, SOS1) under stress conditions. Notably, this study provides the first integrative evidence linking seed quality optimization, antimicrobial storage and priming-induced molecular responses to enhanced thermo-osmotic stress tolerance in H. ovalis. These findings demonstrate that coordinated physiological and molecular acclimation strategies can significantly improve stress resilience in seagrass systems, supporting their application in climate-resilient restoration as nature-based solutions. - Source: PubMed
Publication date: 2026/07/31
Natarajan Praveen KumarDanaraj JeyapragashMariasingarayan YosuvaThomas AiswaryaSenguttuvan SamyukthaUnni Saranya - KRAS G12C, long considered an undruggable oncogenic driver, has become one of the most consequential therapeutic targets in non-small cell lung cancer (NSCLC). The discovery of a cryptic binding pocket accessible in the GDP-bound state enabled covalent inhibitors-sotorasib and adagrasib-that have received regulatory approval for previously treated KRAS G12C-mutant NSCLC, with sotorasib demonstrating PFS and OS superiority over docetaxel in CodeBreaK 200 and adagrasib showing meaningful intracranial activity and a progression-free survival benefit over docetaxel in KRYSTAL-12. Yet response durability is limited by on-target switch-II pocket mutations, upstream RTK and SHP2-mediated bypass signaling, downstream MAPK and PI3K-AKT reactivation, phenotypic plasticity, and adverse modulation by co-occurring STK11, KEAP1, and TP53 alterations. Next-generation covalent inhibitors (divarasib, glecirasib, olomorasib), tri-complex RAS(ON) inhibitors (RMC-6291), pan-KRAS agents, and rationally designed combinations with EGFR, SHP2, SOS1, and PD-1 inhibitors are repositioning KRAS-directed therapy toward earlier lines of treatment. This review integrates the structural, signaling, and clinical biology of KRAS G12C with contemporary trial and real-world evidence to examine the emerging case for first-line KRAS G12C inhibition in genomically defined subsets of NSCLC. First-line use nonetheless remains investigational; platinum-based chemoimmunotherapy remains the standard of care outside of clinical trials, and a frontline indication will require confirmation from randomized phase III trials. - Source: PubMed
Publication date: 2026/07/20
Rosas DanielBarad PriyankaWright JervonRaez Luis