Protein phosphorylation is a versatile posttranslational modification that can regulate nuclear receptor function. Although the precise role of receptor phosphorylation is not fully understood, it appears that it functions to direct or refine receptor activity in response to particular physiological requirements. Identifying and characterizing specific nuclear receptor phosphorylation sites is an important step in elucidating the role(s) receptor phosphorylation plays in function. Although traditional methods of metabolic labeling and in vitro protein phosphorylation have been informative, receptor phosphorylation site-specific antibodies are simple and reliable tools to study receptor phosphorylation. This chapter will discuss how to develop nuclear receptor phosphorylation site-specific antibodies to elucidate function.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1007/978-1-60327-575-0_13 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Acanthoside B attenuates NLRP3-mediated pyroptosis and ulcerative colitis through inhibition of tAGE/RAGE pathway.
Allergol Immunopathol (Madr)
January 2025
Department of Neurofunction, Renmin Hospital, Hubei University of Medicine, Shiyan, Hubei Province, China;
Acanthoside B (Aca.B), a principal bioactive compound extracted from , exhibits superior anti-inflammatory capacity. Ulcerative colitis is a nonspecific inflammatory bowel disease with unknown etiology.
View Article and Find Full Text PDFBackground: The earliest recognized biomarker of AD is deposition of Aβ amyloid that leads to formation of plaques and may, over time, trigger or at least be followed by gliosis/neuroinflammation and neurofibrillary tangles, accompanied by neurodegenerative changes including neuronal and synaptic loss. We have previously reported that semaphorin 4D (SEMA4D), the major ligand of plexin B receptors expressed on astrocytes, is upregulated in diseased neurons during progression of AD and Huntington's disease (HD). Binding of SEMA4D to PLXNB receptors triggers astrocyte reactivity, leading to loss of neuroprotective homeostatic functions, including downregulation of glutamate and glucose transporters (doi:10.
View Article and Find Full Text PDFBackground: Alzheimer's disease (AD) is a progressive neurodegenerative disease whose risk can be assessed in the AT(N) framework based on brain levels of Aβ and pathological tau with or without neuronal injury. This helps determine if a cognitively normal or mildly cognitively impaired (MCI) person has clear signs of AD pathogenesis. The AT(N) framework might be enhanced by also considering brain insulin resistance (BIR), which is a common feature in AD dementia (ADd).
View Article and Find Full Text PDFBiomarkers.
Alzheimers Dement
December 2024
Qingdao Municipal hospital, Qingdao university, Qingdao, Shandong, China.
Background: Complement C1q, the initiator of the classical pathway of the complement system, is activated during Alzheimer's disease (AD) development and progression and is especially associated with the β-amyloid and tau pathology. However, whether C1q influences AD pathology by modulating glial cell communication is unclear.
Method: Alzheimer's Disease Neuroimaging Initiative (ADNI, N = 217) was used to explore the association between cerebrospinal fuid (CSF) C1q, soluble triggering receptor expressed on myeloid cells 2 (sTREM2), Glial fbrillary acidic protein (GFAP), and AD biomarkers.
Biomarkers.
Alzheimers Dement
December 2024
Wake Forest University School of Medicine, Winston-Salem, NC, USA.
Background: The G protein-coupled receptor GPR39 is heavily associated with the pathogenesis of neurologic disorders, including Alzheimer's disease (AD) and related dementia (ADRD). Its dysregulation of zinc 2+ (Zn) processes triggers metallic dyshomeostasis, oxidative stress, neuroinflammation, microtubule destabilization, synaptic dysfunction, and tau phosphorylation-all hallmarks of neurodegeneration. Hence, pharmacologic modulation of GPR39 could offer an effective treatment against AD and ADRD.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!