A5060558708- Mitochondrial Function and Pathology
- Kruppel-like factors research
- Toxin Mechanisms and Immunotoxins
- Genetic Neurodegenerative Diseases
- Neuroinflammation and Neurodegeneration Mechanisms
- Chronic Myeloid Leukemia Treatments
- Myeloproliferative Neoplasms: Diagnosis and Treatment
- T-cell and B-cell Immunology
- Muscle Physiology and Disorders
- Alzheimer's disease research and treatments
- Complement system in diseases
Case Western Reserve University
2018-2024
University Hospitals of Cleveland
2024
Neuronal mitochondria dysfunction and neuroinflammation are two prominent pathological features increasingly realized as important pathogenic mechanisms for neurodegenerative diseases. However, little attempt has been taken to investigate the likely interactions between them. Mitofusin2 (Mfn2) is a mitochondrial outer membrane protein regulating fusion, dynamic process essential function. To explore significance of neuronal in regulation neuroinflammation, male female transgenic mice with...
The involvement of complement in B2 cell responses has been regarded as occurring strictly via components plasma. In this study, we show that Ab production and class switch recombination (CSR) depend on autocrine C3a C5a receptor (C3ar1/C5ar1) signaling cells. CD40 upregulation, IL-6 production, growth response to BAFF or APRIL, AID/Bcl-6 expression, well follicular CD4+ CD21 all depended signal transduction. OVA immunization C3ar1-/-C5ar1-/- mice elicited IgM but no other isotypes, whereas...
The transcription factor Kruppel-like 4 (KLF4) regulates the expression of immunosuppressive and anti-thrombotic proteins. Despite its importance in maintaining homeostasis, signals that control mechanism transactivation remain unclarified. CD55 [aka decay accelerating (DAF)], now known to be a regulator T B cell responses, biases between pro- anti-inflammatory processes by controlling autocrine C3a C5a receptor (C3ar1/C5ar1) signaling cells. similarity CD55’s KLF4’s regulatory effects...