IQGAP1 (IQ Motif Containing GTPase Activating Protein 1)

Furthermore, PRR5 abundance was particularly enriched and correlated with that of phosphorylated ERK in samples from patients with TNBC. Our results highlight cross-talk between mTORC2 and ERK signaling downstream of LINC01133 and PRR5 that may be therapeutically targeted to treat TNBC.

In conclusion, our findings establish GAL3 and PDEδ, two KRAS-associated proteins, as promising combinatorial drug targets. Targeting these modulators provides an effective alternative strategy to overcome resistance mechanisms and enhance the clinical utility of existing KRAS inhibitors.

CircPTPRM can encode circPTPRM-187aa polypeptide. circPTPRM-187aa, regulates the expression of IQGAP1 protein, and up-regulates RAC1 and CDC42 proteins in TGF-β signaling pathway, enhancing the PTC cells proliferation, migration, and invasion.

This activates phosphatidylinositol-4-phosphate-5-kinase (PI5K) to increase local phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2) levels, promoting actin-polymerization and membrane protrusion. Therefore, CD13 is a novel molecular PIP regulator, modulating signal transduction and downstream cellular processes, including actin cytoskeleton dynamics and membrane organization to facilitate intercellular communication.

Our findings illuminate the landscape of disulfidptosis in OS and RMS, revealing a novel immunosuppressive subtype and a defined five-gene signature for risk stratification. The identification of IQGAP1 and the link to macrophages provides new insights for developing targeted therapies and immunotherapeutic strategies for these malignancies.

In conclusion, our findings demonstrate that substrate type modulates multiple aspects of U2OS cell behavior, including morphology, cytoskeletal arrangement, mechanical properties, and microparticle uptake. These results underscore the mechanosensitive nature of osteosarcoma cells and highlight novel roles for microtubule cup-like structures and MAPs, particularly IQGAP1 in cellular uptake mechanisms.

Taken together, these data provide evidence for an emerging proteome with linked PIP n s that represent a PIP n signaling paradigm that is distinct from the membrane-localized pathway but utilizes many of the same PIP kinases and phosphatases. Phosphatidylinositol transfer proteins and PI 4-kinase initiate a PIP n -linked protein network in membrane-free regions.

Notably, specific inhibition of intracellular calcium with BAPTA can also attenuates SYT15B-IQGAP1 complex formation, abrogates MAPK signalling activation, and reverses SYT15B-mediated oncogenic effects. These findings establish the calcium-dependent SYT15B/IQGAP1/MAPK axis as a potential therapeutic and prognostic biomarker in LUAD.

These findings identify STAMBPL1 as a novel oncogenic DUB that promotes GC progression through IQGAP1 stabilization and subsequent activation of JAK2/STAT3 signaling, providing a potential therapeutic target for GC.

This post-translational modification triggered the rearrangement of the actin cytoskeleton in PC cells by altering the transcriptional levels of MYH9, thereby promoting PC malignancy. Overall, our findings demonstrate that neddylation of RNF187 enhances PC malignancy through the IQGAP1/MYH9 axis, suggesting a new therapeutic target for PC.

OCIAD2 drives PDAC progression through binding to IQGAP1, which activates PI3K/AKT pathway; this in turn preserves mitochondrial function and suppresses apoptosis. Our study identifies OCIAD2 as a critical mediator of tumor progression and a potential therapeutic target in PDAC.

By binding receptor tyrosine kinases, small GTPases, and downstream effectors, IQGAP1 modulates oncogenesis, immune evasion, and metabolic imbalance, while contributing to chemoresistance. This review synthesizes advances in IQGAP1's structural domains, disease-specific signaling networks, and therapeutic targeting strategies, emphasizing its translational potential in developing precision therapies for cancer, metabolic syndromes, and immune disorders.