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We began analyzing https://link.springer.com/article/10.1007/s10565-024-09847-8, but it redirected us to https://link.springer.com/article/10.1007/s10565-024-09847-8. The analysis below is for the second page.

Title[redir]:
Deficiency of copper responsive gene stmn4 induces retinal developmental defects | Cell Biology and Toxicology
Description:
As part of the central nervous system (CNS), the retina senses light and also conducts and processes visual impulses. The damaged development of the retina not only causes visual damage, but also leads to epilepsy, dementia and other brain diseases. Recently, we have reported that copper (Cu) overload induces retinal developmental defects and down-regulates microtubule (MT) genes during zebrafish embryogenesis, but whether the down-regulation of microtubule genes mediates Cu stress induced retinal developmental defects is still unknown. In this study, we found that microtubule gene stmn4 exhibited obviously reduced expression in the retina of Cu overload embryos. Furthermore, stmn4 deficiency (stmn4−/−) resulted in retinal defects similar to those seen in Cu overload embryos, while overexpression of stmn4 effectively rescued retinal defects and cell apoptosis occurred in the Cu overload embryos and larvae. Meanwhile, stmn4 deficient embryos and larvae exhibited reduced mature retinal cells, the down-regulated expression of microtubules and cell cycle-related genes, and the mitotic cell cycle arrests of the retinal cells, which subsequently tended to apoptosis independent on p53. The results of this study demonstrate that Cu stress might lead to retinal developmental defects via down-regulating expression of microtubule gene stmn4, and stmn4 deficiency leads to impaired cell cycle and the accumulation of retinal progenitor cells (RPCs) and their subsequent apoptosis. The study provides a certain referee for copper overload in regulating the retinal development in fish. Graphical Abstract

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Keywords {🔍}

stmn, cell, hpf, retinal, zebrafish, embryos, pubmed, expression, cells, google, scholar, mutants, apoptosis, cycle, cas, defects, retina, fig, larvae, developmental, overload, development, study, protein, microtubule, rpcs, genes, central, assays, liu, sox, figs, differentiation, levels, neural, deficiency, reduced, zhang, biol, downregulated, expressions, calculation, data, induces, mrna, copper, stathmin, neuronal, zhao, analysis,

Topics {✒️}

promoting autophagy-lysosome-dependent degradation pou3f1/fam168a/fam168b dna methylation regulating perk1/2-foxm1-mmp2/9 axis anaphase-promoting complex-dependent proteolysis il-lumina hiseq2000 platform de jong-curtain ta prompting hsf1/sp1 aggregation cell cycle-related regulators sds-page loading buffer wnt/notch-hoxb5b signaling rnd3-dependent cytoskeleton remodeling ptc-bearing mrna elicits cell cycle-related proteins rod/core cell markers article download pdf retinal developmental defects central nervous system activity-induced neuronal plasticity cu overload induces unique n-terminal domain cell cycle-related genes neuronal microtubule-regulatory proteins real-time quantitative pcr m-phase naturally leads jing-xia liu exhibited differential expressions stmn4 full-length mrna bmc dev biol mutant mrna degradation cell cycle regulators finally developmental defects full access retinal defects similar privacy choices/manage cookies ciliogenesis developmental biology anti-stress pathway cell cycle progression copper nanoparticle toxicology developmental defects observed touch response defects impaired cell cycle stmn4−/− embryos induces myelin basic protein normal locomotor behavior m-phase arrested rpcs anaphase-promoting complex mol biol cell stem-cell niche stem cell niche cell cycle arrests

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         description:As part of the central nervous system (CNS), the retina senses light and also conducts and processes visual impulses. The damaged development of the retina not only causes visual damage, but also leads to epilepsy, dementia and other brain diseases. Recently, we have reported that copper (Cu) overload induces retinal developmental defects and down-regulates microtubule (MT) genes during zebrafish embryogenesis, but whether the down-regulation of microtubule genes mediates Cu stress induced retinal developmental defects is still unknown. In this study, we found that microtubule gene stmn4 exhibited obviously reduced expression in the retina of Cu overload embryos. Furthermore, stmn4 deficiency (stmn4−/−) resulted in retinal defects similar to those seen in Cu overload embryos, while overexpression of stmn4 effectively rescued retinal defects and cell apoptosis occurred in the Cu overload embryos and larvae. Meanwhile, stmn4 deficient embryos and larvae exhibited reduced mature retinal cells, the down-regulated expression of microtubules and cell cycle-related genes, and the mitotic cell cycle arrests of the retinal cells, which subsequently tended to apoptosis independent on p53. The results of this study demonstrate that Cu stress might lead to retinal developmental defects via down-regulating expression of microtubule gene stmn4, and stmn4 deficiency leads to impaired cell cycle and the accumulation of retinal progenitor cells (RPCs) and their subsequent apoptosis. The study provides a certain referee for copper overload in regulating the retinal development in fish.
         datePublished:2024-01-22T00:00:00Z
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      headline:Deficiency of copper responsive gene stmn4 induces retinal developmental defects
      description:As part of the central nervous system (CNS), the retina senses light and also conducts and processes visual impulses. The damaged development of the retina not only causes visual damage, but also leads to epilepsy, dementia and other brain diseases. Recently, we have reported that copper (Cu) overload induces retinal developmental defects and down-regulates microtubule (MT) genes during zebrafish embryogenesis, but whether the down-regulation of microtubule genes mediates Cu stress induced retinal developmental defects is still unknown. In this study, we found that microtubule gene stmn4 exhibited obviously reduced expression in the retina of Cu overload embryos. Furthermore, stmn4 deficiency (stmn4−/−) resulted in retinal defects similar to those seen in Cu overload embryos, while overexpression of stmn4 effectively rescued retinal defects and cell apoptosis occurred in the Cu overload embryos and larvae. Meanwhile, stmn4 deficient embryos and larvae exhibited reduced mature retinal cells, the down-regulated expression of microtubules and cell cycle-related genes, and the mitotic cell cycle arrests of the retinal cells, which subsequently tended to apoptosis independent on p53. The results of this study demonstrate that Cu stress might lead to retinal developmental defects via down-regulating expression of microtubule gene stmn4, and stmn4 deficiency leads to impaired cell cycle and the accumulation of retinal progenitor cells (RPCs) and their subsequent apoptosis. The study provides a certain referee for copper overload in regulating the retinal development in fish.
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