KLHL31 (Kelch Like Family Member 31)

Mechanistically, decreased oar-miR-125b expression relieves its repression of TNFSF4, leading to NF-κB pathway activation and blood-brain barrier disruption. Collectively, our results demonstrate that oar-miR-125b serves as a key anti-inflammatory regulator in bacterial meningitis by targeting TNFSF4 and constraining NF-κB signaling, highlighting its potential as a therapeutic target for attenuating neuroinflammation in meningitis.

Moreover, our results suggest that O-GlcNAcylation affects WNK4 function in both osmolarity control and ferroptosis, with potential implications ranging from blood pressure regulation to neuronal health and survival. This work demonstrates the functional regulation of the KLHL3/WNK axis by O-GlcNAcylation and supports a broader model of O-GlcNAc serving as a general regulator of KLHL signaling and proteostasis.

Furthermore, analysis from the Gene Expression Omnibus database indicated that KLHL5 expression was more pronounced in the common molecular subtype (CMS) 4 CRC, which is characterized as highly advanced, and the overall and recurrence-free survival rates were poor compared to other CMS groups. Our findings indicate that KLHL5 plays a pivotal role in the progression and development of CRC, and can be used as a potential biomarker and therapeutic target for CRC treatment.

This review provides a comprehensive overview of the physiological and pathological roles of KLHL proteins, emphasizing their specific substrates and mechanisms of action. By integrating structural and mechanistic insights with translational research, this review underscores the potential of KLHL proteins as promising therapeutic targets, offering new opportunities to combat a wide spectrum of complex diseases.

Moreover, our results suggest that O-GlcNAcylation affects WNK4 function in both osmolarity control and ferroptosis, with potential implications ranging from blood pressure regulation to neuronal health and survival. This work demonstrates the functional regulation of the KLHL3/WNK axis by O-GlcNAcylation and supports a broader model of O-GlcNAc serving as a general regulator of KLHL signaling and proteostasis.

Autoimmune brainstem encephalitis is a distinct clinical subphenotype of autoimmune encephalitis. Abnormal brain MRI, bulbar symptoms, and elevated CSF-IgG index associate with poor outcome.

In fact, TGF-β promotes de novo synthesis, increases protein stability and induces nuclear-cytoplasmic shuttling of KLHL14. Collectively, this research is an important step further to decipher KLHLs mechanism of action and further contributes to the understanding of the molecular mechanisms regulating MM.

The patient was diagnosed as GAD65 associated cerebellar ataxia and treated with corticosteroid and rituximab...Early diagnosis and therapy are challenging but imperative. Further studies are required in regard to therapeutic management.

Additionally, we found that the presence of Cul3 enhances the stability and homogeneity of KLHL6 by forming a complex. Consequently, the successful expression and purification of full-length KLHL6 serve as a foundation for further investigations into the structure and function of the KLHL6/Cullin3/Rbx1 substrate complex, as well as provide a potential strategy for studying other proteins within the KLHL family that possess similar characteristics.

The therapeutic approach to paraneoplastic neurologic disorders is centered around cancer care and trials of immune therapy. The field of paraneoplastic neurologic disorders continues to be advanced by the identification of novel antibody biomarkers which have diagnostic utility, and give insight into likely treatment responses and outcomes.

The effect of KIAA1522 on HCC may entail cell cycle alteration, an immunological response, and suppression of the PPAR signaling pathway. High expression of KIAA1522 was linked to HCC immune cell infiltration, disease progression, and a poor prognosis.

Therefore, KLHL proteins should be taken into consideration for targeted therapy strategy discovery. This review summarizes the current knowledge of KLHL proteins in gastrointestinal tumors and discusses the potential of KLHL proteins as potential drug targets and prognostic biomarkers.