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High diversity and differential evolution profiles have been observed for DD34E/ Tc1 transposons; several families originating from these groups, such as DD34E/ ZB , DD34E/ SB , DD35E/ TR , DD36E/ IC, and DD38E/ IT , have been well defined. Even though Frisky , Tiang , Tsessebe, and Topi transposons have been identified in Anopheles gambiae , their taxonomic distribution and phylogenetic relationship in nature remain largely unknown. The evolutionary profiles of Frisky , Tiang , Tsessebe , and Topi homology transposons were investigated in the current study. In total, 254 homology transposons of Frisky , Tiang , Hob , Tsessebe, and Topi were obtained in 200 species by data mining. The phylogenetic tree revealed that these transposons were classified into five main clades (Frisky , Tiang , Hob , Tsessebe , and Topi) forming a monophyletic clade with 98% bootstrap support, belonging to the DD34E/ Tc1 group, and named as Skipper (SK). SK transposons show a wide distribution in animals; however, differential taxonomic distribution patterns were observed for the subfamilies of Frisky , Tiang , Hob , Tsessebe, and Topi ; extensive invasion of Frisky in animals was found, whereas Tiang , Hob , Tsessebe, and Topi were mainly detected in Diptera. SK elements share a similar structural organization and display high sequence identities across subfamilies. Evolutionary dynamics and structural analysis revealed that SK s in some species, such as Bombyx mori , Lordiphosa magnipectinata , Carassius gibelio , Triplophysa dalaica , and Silurus glanis , have recently evolved and present as intact copies, indicating that SK s in these genomes may be active. Together, these observations improve our understanding of the diversity of DD34E/ Tc1 transposons and their impacts on genome evolution in animals. [ABSTRACT FROM AUTHOR]

AIM: To investigate the role of Ywhab in the growth of mouse B-cell lymphoma, and to explore the potential underlying mechanisms. METHODS : The correlation between Ywhab and human diffuse large B-cell lymphoma (DLBCL) was investigated by bioinformatics analysis. Infection with retroviral vector was performed to establish stable mouse B-cell lymphoma 38B9 cell line with overexpression of Ywhab gene, which was verified by RT-qPCR and Western blot. The impact of Ywhab overexpression on 38B9 cell growth both in vitro and in vivo was detected by cell counting, CCK-8 assay, and subcutaneous tumor loading experiments. The expression of apoptosis-related proteins was detected by RT-qPCR and Western blot. Co-immunoprecipitation combined with mass spectrometry (CoIP-MS) was employed to search for proteins specifically binding to Ywhab gene product 14-3-3β, which was confirmed by Western blot and molecular docking analysis. RESULTS: The Ywhab gene exhibited low expression in DLBCL, which was correlated with poor clinical prognosis of DLBCL patients. Compared with normal mouse bone marrow B cells, Ywhab expression was low in 38B9 cells. Overexpression of Ywhab induced apoptosis of 38B9 cells both in vitro and in vivo, promoted the expression of pro-apoptotic proteins Puma, Noxa and Bax at both mRNA and protein levels, and inhibited the mRNA and protein expression of anti-apoptotic protein Bcl2 (P<0. 05). The 14-3-3β protein specifically bound to Hsp90aa1 and reduced Hsp90aa1 protein levels, thereby suppressing the growth of 38B9 cells. CONCLUSION: Ywhab promotes the apoptosis of B-cell lymphoma cells by binding to Hsp90aa1 and thereby inhibiting the function of Hsp90aa1. [ABSTRACT FROM AUTHOR]

The nuclear factor erythroid 2-related factor 2 (NRF2) is a transcription factor crucial in cellular defense against oxidative and electrophilic stresses. Recent research has highlighted the significance of NRF2 in normal erythropoiesis and anemia. NRF2 regulates genes involved in vital aspects of erythroid development, including hemoglobin catabolism, inflammation, and iron homeostasis in erythrocytes. Disrupted NRF2 activity has been implicated in various pathologies involving abnormal erythropoiesis. In this review, we summarize the progress made in understanding the mechanisms of NRF2 activation in erythropoiesis and explore the roles of NRF2 in various types of anemia. This review also discusses the potential of targeting NRF2 as a new therapeutic approach to treat anemia. [Display omitted] • NRF2 is essential for erythroid homeostasis. • NRF2 protein stability is regulated by interactions with KEAP1 and other factors. • The expression of NRF2 during erythroid development is dynamic. • Targeting NRF2 offers potential therapeutic benefits for anemia treatment. [ABSTRACT FROM AUTHOR]