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Gene Targeting Models of Epilepsy: Technical and Analytical Considerations
Published in Steven L. Peterson, Timothy E. Albertson, Neuropharmacology Methods in Epilepsy Research, 2019
In some cases, epilepsy syndromes have resulted from disruptions of genes that have not been previously implicated in neurotransmission. One particularly serendipitous example of this is the recent report of the jerky mouse.20 These animals resulted from an effort to generate transgenic mice bearing the SV40 large T antigen. The offspring of one particular transgenic founder mouse displayed handling-induced behaviors manifested by whole body jerks and generalized clonic seizures. Chronic recordings revealed large-amplitude interictal spikes in the dentate gyrus and spike-and-wave patterns in the neocortex. Molecular and genetic analysis revealed that the phenotype resulted not from the introduction of the SV40 antigen perse, but from the disruption produced by its insertion. The transgene had integrated into a novel gene termed jerky, producing an unintended jerky knockout. The increased seizure susceptibility of mice heterozygous for this genetic perturbation revealed it to be a dominant mutation. Jerky was found to be ubiquitously expressed in all tissues examined. The gene encodes a putative 60-kDa protein of 509 amino acids that is homologous to the mouse centromere binding protein and to the yeast autonomously replicating sequence-binding protein, indicating a possible function as a DNA binding protein. The mechanism through which the disruption of this protein alters seizure susceptibility remains to be determined.
Yin and yang of immunological memory in controlling infections: Overriding self defence mechanisms
Published in International Reviews of Immunology, 2022
Roshan Kumar Roy, Rakhi Yadav, Aklank Jain, Vishwas Tripathi, Manju Jain, Sandhya Singh, Hridayesh Prakash
In context of the memory B cell differentiation, Sequencing studies and high through put genomic analysis of memory B cells revealed that specific transcription factors like ZBTB32 (Zinc Finger and BTB Domain Containing 32), ABF-1 (Autonomously replicating sequence (ARS)-binding factor 1), KLF2 (Kruppel Like Factor 2), STAT5 (Signal transducer and activator of transcription 5), and Bach2 9 (BTB Domain and CNC Homolog 2) are important for memory B cells. Out of these, Bach2 expressed in memory B cells suppress prdm1 (PR/SET Domain 1) that encodes Blimp-1 and pro-apoptotic factors like Bim (BCL-2 interacting mediator of cell death) and Puma (p53 upregulated modulator of apoptosis), thereby promoting the survival of memory B cell. Apart from transcription factors, specific cytokines like IL-9, IL-6, BAFF (B cell activating factor/BLyS), APRIL (A proliferation inducing ligand), CXCL12, and fibronectin of bone marrow also contribute to the maturation and maintenance of long-lived plasma cells [23], as shown in Figure 2