P4HA2 hydroxylates SUFU to regulate the paracrine Hedgehog signaling and promote B-cell lymphoma progression.

Aberrations in the Hedgehog (Hh) signaling pathway are significantly prevailed in various cancers, including B-cell lymphoma. A critical facet of Hh signal transduction involves the dynamic regulation of the suppressor of fused homolog (SUFU)-glioma-associated oncogene homolog (GLI) complex within the kinesin family member 7 (KIF7)-supported ciliary tip compartment. However, the specific post-translational modifications of SUFU-GLI complex within this context have remained largely unexplored.

Registered Clinical Trials Comprising Pregnant Women in China: A Cross-Sectional Study.

In this study, an investigation was conducted on clinical drug trials comprising pregnant women in China that provided data on the quantity, properties, source of funding, and geographical distribution regarding registration and post-marketing studies. We conducted a cross-sectional descriptive study of clinical trials of pregnant women in China on 30 December 2021, and it was registered on the official Drug Clinical Trial Information Management Platform (ChiCTR) (http://www.chinadrugtrials.

Alzheimer's Model Develops Early ADHD Syndrome.

We describe the first invertebrate model of attention deficit hyperactivity disorder (ADHD) that reproduces its major features, including hyperactivity, male predominance, marked exacerbation by simple carbohydrates, reversible response to dextroamphetamine, and a "paradoxical response" to stimulants. This model may offer new insight into ADHD pathogenesis and treatment. Furthermore, these findings are of particular interest in light of the recent epidemiological evidence showing that patients with dementia have a high frequency of antecedent ADHD symptoms.

DJ-1 promotes the proteasomal degradation of Fis1: implications of DJ-1 in neuronal protection.

Mutations in DJ-1/PARK7 (Parkinson protein 7) have been identified as a cause of autosomal-recessive PD (Parkinson's disease) and the antioxidant property of DJ-1 has been shown to be involved in the regulation of mitochondrial function and neuronal cell survival. In the present study, we first found that the DJ-1 transgene mitigated MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine)-induced DA (dopamine) neuron cell death and cell loss. We then observed that the protein levels of DJ-1 were significantly decreased, whereas levels of Fis1 [fission 1 (mitochondrial outer membrane) homologue] were noticeably increased in the striatum of MPTP-treated mice.

Uif, a large transmembrane protein with EGF-like repeats, can antagonize Notch signaling in Drosophila.

Background: Notch signaling is a highly conserved pathway in multi-cellular organisms ranging from flies to humans. It controls a variety of developmental processes by stimulating the expression of its target genes in a highly specific manner both spatially and temporally. The diversity, specificity and sensitivity of the Notch signaling output are regulated at distinct levels, particularly at the level of ligand-receptor interactions.

To prevent neurodegeneration: HDAC6 uses different strategies for different challenges.

Neurodegenerative diseases are characterized by progressive dysfunction and death of neurons in specific areas of the nervous system. Loss of neurons is often associated with multiple stresses such as abnormal aggregation of misfolded proteins, deficiency of protein degradation system, mitochondrial dysfunction and excessive oxidative products. HDAC6 has recently been suggested to be an integral factor that copes with these stresses.

Drosophila Smt3 negatively regulates JNK signaling through sequestering Hipk in the nucleus.

Post-translational modification by the small ubiquitin-related modifier (SUMO) is important for a variety of cellular and developmental processes. However, the precise mechanism(s) that connects sumoylation to specific developmental signaling pathways remains relatively less clear. Here, we show that Smt3 knockdown in Drosophila wing discs causes phenotypes resembling JNK gain of function, including ectopic apoptosis and apoptosis-induced compensatory growth.

Drosophila histone deacetylase 6 protects dopaminergic neurons against {alpha}-synuclein toxicity by promoting inclusion formation.

Parkinson's disease (PD) is associated with progressive degeneration of dopaminergic (DA) neurons. We report for the first time that the Drosophila histone deacetylase 6 (dHDAC6) plays a critical role in the protection of DA neurons and the formation of alpha-synuclein inclusions by using a Drosophila PD model constructed by ectopic expression of human alpha-synuclein. Depletion of dHDAC6 significantly enhances the effects caused by ectopic expression of alpha-synuclein, namely, loss of DA neurons, retinal degeneration, and locomotor dysfunction.