Topic: DNA damage response

Fragile X Syndrome (FXS), a frequent form of inherited intellectual disability and a leading monogenic cause of autism, is caused by lack/reduction of fragile X mental retardation protein (FMRP), an RNA-binding protein involved in several aspects of RNA metabolism. Abnormal expression of proteins at synapses underlies brain dysfunction in FXS. FMRP is also implicated in DNA damage response and is a component of stress granules (SGs), cytoplasmatic aggregates that form in response to stress and are protective against apoptosis. Evidence in the mouse model of FXS suggests an excess of oxidizing

Proper interneuron migration and distribution are essential for optimal brain function. Disruptions of this process can impair the excitation/inhibition balance, leading to neurodevelopmental disorders. As such, ionizing radiation poses a particular risk to the developing brain, as it can lead to excessive fetal DNA damage and subsequent microcephaly. Although research on radiation-induced microcephaly has mainly focused on glutamatergic excitatory neurons, the impact on GABAergic interneurons is equally crucial. Understanding potential disruptions is essential for comprehensive insights into

UFM1 is an understudied ubiquitin-like modifier. Like ubiquitin, UFM1 is covalently conjugated to substrate proteins. The conjugation of UFM1 (UFMylation) is reversible, and this is mediated by UFSP2. UFMylation has been linked to important biological pathways such as the DNA damage response, the unfolded protein response, and autophagy. UFMylation is also crucial for healthy brain development, however a role of UFM1 for age-related brain diseases such as Alzheimer’s disease (AD) has not been established. Considering that pathological tau plays a critical role for AD, and has a physiological r

Introduction:The glycoprotein clusterin (CLU) plays a pivotal role in vital cellular functions, including cell proliferation and DNA damage repair. Its frequent overexpression in tumor cells, particularly in gliomas, positions it as a promising therapeutic target. This study aims to investigate the impact of CLU dysregulation on glioma cell lines and explore its therapeutic potential. Methods:Two human astrocytic cell lines, CCF-STTG1 astrocytoma cells, and SV-40 immortalized normal human astrocytes, were utilized in our investigation. CLU expression was suppressed using transient siRNA transf