IRS1 (Insulin Receptor Substrate 1)

After restricting the analysis to the gonadotroph PitNET group, tumors with an IRS of 1-2 showed significantly higher invasiveness compared with those with an IRS of 3-6 (p = 0.012). These findings suggest that mE-cad may serve as a biomarker of PitNET invasiveness, with expression varying according to TF lineage and tumor subtype.

Inhibition of N-terminal acetyltransferase C prevents ER stress-induced muscle wasting via the downregulation of CTSK and subsequent activation of the anabolic pathway. This suggests that N-terminal acetyltransferase C is a potential therapeutic target for combating muscle wasting in cancer cachexia.

Mo-Rubbing abdominal effectively ameliorates T2DM symptoms and systemic metabolic dysregulation by activating the GLP1-GLP1R-IRS1/AMPK/mTOR pathway, particularly in the jejunum. These findings support Mo-Rubbing abdominal as a promising non-pharmacological intervention for T2DM, with potential benefits for preventing diabetes-associated complications.

Moreover, we elucidated the molecular mechanism through which the pre-B-cell leukemia transcription factor 1-insulin receptor substrate 1 signaling axis sustains metabolic homeostasis. Furthermore, we demonstrated that the blood-brain barrier-permeable trans-activator of transcription-pre-B-cell leukemia transcription factor 1 fusion protein constitutes a mechanistically innovative and highly translatable therapeutic strategy for Alzheimer's disease.

These assessments were conducted under basal conditions and following treatment with either tumor necrosis factor alpha (TNF-α) to induce insulin resistance or metformin to promote insulin sensitivity...This highlights the role of impaired adipogenesis in the pathogenesis of insulin resistance among non-obese individuals. Further research is needed to understand the impact of impaired adipogenesis and the potential therapeutic interventions targeting adipogenesis to improve insulin sensitivity in non-obese individuals.

EA at GV16, LR3, and ST36 can effectively improve the bradykinesia of PD model mice induced by MPTP, increase the expression level of TH in the substantia nigra, and improve the insulin signaling dysfunction. Its mechanism may be related to the regulation of the IGF-1R/IRS-1/PI3K/AKT signaling pathway and the subsequent inhibition of the neuroinflammatory response.

CAFs-derived exosomal miR-3126-5p enhanced glycolysis of NSCLC cells via targeting KLF13. KLF13 led to transcriptional inhibition of SH2B1 in NSCLC cells. SH2B1 interplayed with IRS1 to facilitate glycolysis of NSCLC cells. IRS1 promoted glycolysis of NSCLC cells via the activation of PI3K/AKT pathway.

In contrast, RS28 showed further increases in IL-1β, TNF-α, and phospho-IRS-1 at Ser307, along with altered FST (swimming, climbing, immobility times) and TST (immobility latency/time) parameters compared with all other groups (P < 0.05). These findings suggest that increased serum phospho-IRS-1 at Ser307 may serve as a biomarker for stress-induced depressive-like behaviors.

This study highlights both converging and disease-specific mutation profiles in oral cancer and diabetes. It demonstrates the value of public datasets and accessible platforms for identifying potential functional variants, which warrant further validation in larger cohorts.

tRF-23 suppresses the malignant progression of pancreatic cancer by downregulating IRS1. These findings suggest that the tRF-23/IRS1 axis could act as a prospective therapeutic target in pancreatic cancer.

Cross-sectionally, p-IRS1 correlated inversely with SSPG concentration, BMI and leptin, suggesting compensatory brain-periphery coupling. These findings indicate that NDE-based markers capture a dimension of brain metabolic vulnerability distinct from classical peripheral measures.

Mechanistically, FBXW8 bound to IRS1 and promoted its ubiquitination, thereby accelerating its degradation. These findings provide a mechanistic rationale for co-targeting IRS1 and autophagy-associated macromolecular complexes to overcome therapeutic resistance in PAAD.