HAND 发表于 2025-3-21 16:05:57
书目名称Genome Editing in Neurosciences影响因子(影响力)<br> http://figure.impactfactor.cn/if/?ISSN=BK0382839<br><br> <br><br>书目名称Genome Editing in Neurosciences影响因子(影响力)学科排名<br> http://figure.impactfactor.cn/ifr/?ISSN=BK0382839<br><br> <br><br>书目名称Genome Editing in Neurosciences网络公开度<br> http://figure.impactfactor.cn/at/?ISSN=BK0382839<br><br> <br><br>书目名称Genome Editing in Neurosciences网络公开度学科排名<br> http://figure.impactfactor.cn/atr/?ISSN=BK0382839<br><br> <br><br>书目名称Genome Editing in Neurosciences被引频次<br> http://figure.impactfactor.cn/tc/?ISSN=BK0382839<br><br> <br><br>书目名称Genome Editing in Neurosciences被引频次学科排名<br> http://figure.impactfactor.cn/tcr/?ISSN=BK0382839<br><br> <br><br>书目名称Genome Editing in Neurosciences年度引用<br> http://figure.impactfactor.cn/ii/?ISSN=BK0382839<br><br> <br><br>书目名称Genome Editing in Neurosciences年度引用学科排名<br> http://figure.impactfactor.cn/iir/?ISSN=BK0382839<br><br> <br><br>书目名称Genome Editing in Neurosciences读者反馈<br> http://figure.impactfactor.cn/5y/?ISSN=BK0382839<br><br> <br><br>书目名称Genome Editing in Neurosciences读者反馈学科排名<br> http://figure.impactfactor.cn/5yr/?ISSN=BK0382839<br><br> <br><br>aristocracy 发表于 2025-3-21 22:57:13
Aquatic Model Organisms in Neurosciences: The Genome-Editing Revolution,Cas9 in laboratories. Because of the simplicity and broad applicability of this later system, knock-out is now efficiently performed at medium scale. Forward genetics in zebrafish can now be performed by CRISPR-based F0 screening using high speed and high content phenotyping for example by confocal关心 发表于 2025-3-22 00:41:59
Genome-Wide Genetic Screening in the Mammalian CNS,go, but neither a full molecular explanation for the cell loss seen in human patients nor a curative therapy has yet been achieved for any of these diseases. In most model organisms, when new hypotheses are needed to explain a cellular process, genetic screens are the tool of choice. For example, ‘s聪明 发表于 2025-3-22 05:41:39
CRISPR/Cas9-Mediated Knockin and Knockout in Zebrafish,ely small size, rapid external development and translucency. These features allow the easy application of in vivo microscopy analysis and optical perturbation of neuronal function. So far, genetic manipulation in zebrafish has been limited to the generation of constitutive loss-of-function alleles a陈旧 发表于 2025-3-22 11:09:15
Dissecting the Role of Synaptic Proteins with CRISPR,ion of the role of single proteins or, more significantly, their subunits and sub-domains has increased enormously the basic knowledge of synaptic function. CRISPR/Cas9 is a recently developed genome-editing tool that can be used to inactivate or modify genes of interest. Its ease of implementation旧式步枪 发表于 2025-3-22 14:13:38
Recurrently Breaking Genes in Neural Progenitors: Potential Roles of DNA Breaks in Neuronal Functio is required for development of the immune and nervous system. We hypothesize that proper repair of neural DSBs via C-NHEJ or other end-joining pathways is critical for neural functionality and homeostasis over time and that improper DSB repair could contribute to complex psychiatric and neurodegene旧式步枪 发表于 2025-3-22 19:45:15
Neuroscience Research Using Non-human Primate Models and Genome Editing,omedical researchers and neuroscientists for its ease of handling and colony maintenance, unique behavioral characteristics, and several human-like traits, such as enriched social vocal communication and strong relationships between parents and offspring. Its high reproductive efficiency makes it pa多嘴多舌 发表于 2025-3-22 23:34:53
http://reply.papertrans.cn/39/3829/382839/382839_8.pngGoblet-Cells 发表于 2025-3-23 04:56:47
,Using Genome Engineering to Understand Huntington’s Disease,o an expanded polyglutamine (polyQ) region in the encoded protein HTT. We have used homologous recombination (HR) to genetically correct HD patient-derived induced pluripotent stem cells (iPSCs) and found that this reversed HD disease phenotypes. We have utilized exploited genome editing tools inclu认识 发表于 2025-3-23 06:12:41
Therapeutic Gene Editing in Muscles and Muscle Stem Cells,n the . gene that prevent expression of its encoded protein, Dystrophin (Burghes et al. Nature 328:434–437, 1987). Interestingly, patients with . mutations that delete certain segments of the Dystrophin coding region, but maintain protein reading frame, have a much milder form of the disease, known