Topic: cell proliferation

The development of autism spectrum disorder (ASD) is strongly influenced by genetic factors. To navigate the large number of genes associated with the disorder, recent efforts have been directed towards finding functional convergence among ASD-risk genes. Within the biological processes commonly affected in ASD, cell proliferation is of particular interest, given the occurrence of brain volume anomalies in a significant subset of the ASD population. Since neural stem cells are key players in the expansion of neural cell pools throughout development, we hypothesized that a group of ASD-risk gen

Glioblastoma, a highly aggressive brain tumor, poses a formidable challenge due to factors such as angiogenesis, diverse mutations, and evasion of apoptosis. Nitric oxide (NO) plays multifaceted roles in physiological processes, including vasodilation, blood pressure regulation, neurotransmission, and immune response. In the context of glioblastoma, understanding the interaction between NO and tumor cells is crucial. Our study utilizes human and mouse glioblastoma stem cells to investigate how NO influences cell proliferation.We modulate NO activity by either enhancing (using SNAP) or inhibiti

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