Restoration of Hair Luster via Novel Biomarker COL7A1 by Minoxidil, Caffeine, and Biotin.

Hair luster, a key component of visual hair quality, depends largely on the integrity of the cuticle. While cosmetic products offer temporarily enhanced luster, their effects are limited due to a poor understanding of the underlying molecular mechanisms. In this study, we employed a UVB-induced mouse model of hair luster loss to identify differentially expressed genes via quantitative real-time reverse transcription PCR.

Quantitative Analysis of Hair Luster in a Novel Ultraviolet-Irradiated Mouse Model.

Hair luster is a key attribute of healthy hair and a crucial aspect of cosmetic appeal, reflecting the overall health and vitality of hair. Despite its significance, the advancement of therapeutic strategies for hair luster enhancement have been limited due to the absence of an effective experimental model. This study aimed to establish a novel animal model to assess hair gloss, employing ultraviolet (UV) irradiation on C57BL/6 mice.

Deubiquitinating enzyme YOD1 deubiquitinates and destabilizes α-synuclein.

α-synuclein is one of the proteins involved in degenerative neuronal diseases such as Parkinson's disease (PD) or Lewy body dementia (LBD). The pathogenesis is imparted by the abnormal accumulation of α-synuclein resulting in the formation of a Lewy body (LB) and exerting neurotoxicity via an unknown mechanism. Regulation of α-synuclein is achieved by the ubiquitin-proteasome system (UPS), which influences protein homeostasis via inducing proteasome-dependent degradation by attaching a small molecule (ubiquitin) to the substrate.

Protein phosphatase 2A regulated by USP7 is polyubiquitinated and polyneddylated.

Ubiquitin‑specific protease 7 (USP7) participates in the ubiquitin‑proteasome system (UPS), and is considered an essential regulator of substrate stability in cancers. In a previous study, the substrates that bind to USP7 were separated through two‑dimensional electrophoresis (2‑DE), which resulted in the identification of protein phosphatase 2A (PP2A) through matrix‑assisted laser desorption‑ionization time‑of‑flight mass spectrometry (MALDI‑TOF/MS) analysis. In the present study, GST pull‑down assay was performed to determine whether USP7 and PP2A directly bind to each other.

Cellular functions regulated by deubiquitinating enzymes in neurodegenerative diseases.

Neurodegenerative diseases are one of the most common diseases in mankind. Although there are reports of several candidates that cause neurodegenerative diseases, the exact mechanism of pathogenesis is poorly understood. The ubiquitin-proteasome system (UPS) is an important posttranslational modification for protein degradation and control of homeostasis.

SCF-Slimb is critical for Glycogen synthase kinase-3β-mediated suppression of TAF15-induced neurotoxicity in Drosophila.

Amyotrophic lateral sclerosis (ALS) is a severe neurodegenerative disorder characterized pathologically by motor neuron degeneration and associated with aggregation of RNA-binding proteins. TATA-binding protein-associated factor 15 (TAF15) accumulates as cytoplasmic aggregates in neuronal cells, and clearance of these aggregates is considered a potential therapeutic strategy for ALS. However, the exact pathogenic mechanism of TAF15-induced neurotoxicity remains to be elucidated.

The Model: Exploring Novel Therapeutic Compounds against Neurodegenerative Diseases.

Polyphenols are secondary metabolites of plants, fruits, and vegetables. They act as antioxidants against free radicals from UV light, pathogens, parasites, and oxidative stress. In models, feeding with various polyphenols results in increased antioxidant capacity and prolonged lifespan.