CRISPR Geneome Editing Blogger - CRISPR Gene Editing New - EDITGENE

NRAS (neuroblastoma RAS viral oncogene homolog) is one of the three members of the RAS proto-oncogene family, together with HRAS and KRAS. It encodes a small GTPase protein with a molecular weight of approximately 21 kDa, which plays a central role in transmitting signaling pathways involved in cell proliferation, differentiation, and survival. RAS family genes represent some of the most frequently mutated oncogenes in human cancers. Comprehensive analyses estimate that approximately 19% of cancer patients harbor mutations in at least one RAS gene, with KRAS mutations being the most prevalent, followed by NRAS and HRAS mutations. Compared with KRAS, NRAS mutations exhibit a more restricted distribution among specific tumor types, with particularly high frequencies observed in melanoma, multiple myeloma, and acute myeloid leukemia (AML). NRAS mutations typically result in constitutive activation of the N-Ras protein, leading to persistent activation of key downstream signaling pathways,...

What is G6PD? An Overview of the Gene, Enzyme, and Oxidative Stress Pathway Glucose-6-phosphate dehydrogenase (G6PD) is a critical metabolic enzyme encoded by the G6PD gene. It functions as the first and rate-limiting enzyme in the pentose phosphate pathway (PPP), a metabolic route that serves as a central hub for cellular antioxidant defense and nucleotide synthesis. G6PD catalyzes the oxidation of glucose-6-phosphate, generating two essential products: NADPH, the primary source of reducing power for cellular redox balance, and ribose-5-phosphate, a key precursor for nucleotide biosynthesis. NADPH is indispensable for regenerating reduced glutathione (GSH), which directly determines a cell’s ability to neutralize oxidative stress. Consequently, proper G6PD activity is essential for maintaining erythrocyte integrity and supports the unique metabolic demands of tumor cells. The G6PD gene is located on the X chromosome (Xq28). More than 230 point mutations have been identified, and appro...

KRAS is one of the most frequently mutated oncogenes in human cancers, yet different mutation subtypes (G12C, G12D, G12V, G13D, etc.) exhibit significant differences in oncogenic potential, signaling pathway preferences, and drug sensitivity. The approval of the first G12C inhibitor in 2021 ushered in a new era of precision targeting of KRAS. Understanding allele-specific functions, screening sensitive drugs, and dissecting resistance mechanisms all rely on isogenic cell models with consistent genetic backgrounds. This article systematically reviews the clinical significance and therapeutic breakthroughs of major KRAS mutation subtypes, and introduces EDITGENE’s off-the-shelf cell lines with KRAS point mutation in HCT116 and LLC, built on the Bingo™ PE7 platform .  These ready-to-ship cell lines provide academic institutes and pharmaceutical companies with ideal tools ranging from in vitro screening to in vivo efficacy evaluation. KRAS mutation spectrum: heterogeneous distribution...

The TP53 gene , also known as the p53 gene, is one of the most critical tumor suppressor genes in the human genome. Discovered in 1979 and recognized for its tumor-suppressive function in 1989, TP53 has since been regarded as the “guardian of the genome” and remains a central focus of cancer research. Under normal physiological conditions, the TP53 gene functions as a tightly regulated stress-response hub . The p53 protein encoded by the TP53 gene is constantly produced but also rapidly degraded. Upon DNA damage, replication stress, or metabolic imbalance, p53 becomes stabilized and activated, allowing it to orchestrate cell fate decisions. Rather than simply inducing apoptosis, p53 exerts a context-dependent regulatory role: In response to mild damage, p53 induces cell cycle arrest through transcriptional activation of targets such as p21, allowing time for DNA repair. Under moderate stress, p53 promotes DNA repair pathways and antioxidant responses. When damage is irreversible, ...

In a healthy state, cell growth, division, and death are precisely regulated. However, when key regulatory pathways malfunction, cells may escape this "command system," proliferating continuously and evading immune clearance, ultimately leading to disease—particularly tumors. As one of the world's leading malignancies, lung cancer has a complex pathogenesis rooted in the imbalance of cell growth regulatory systems. These imbalances are often genetic. For instance,  EGFR point mutations  allow the EGFR protein to activate automatically without the need for external ligand stimulation, magnifying downstream signals and leading to uncontrolled cell proliferation. EGFR is a receptor tyrosine kinase located on the cell membrane that regulates cell proliferation, differentiation, and survival across various tissues. Under normal conditions, when growth factors bind to EGFR, it triggers receptor dimerization and activates its kinase activity. This initiates a series of...

  CRISPR library screening   is a powerful high-throughput method for gene analysis, leveraging the CRISPR/Cas9 system. This approach involves constructing a library containing thousands of sgRNAs, which are inserted into lentiviral vectors and used to infect target cells at a low multiplicity of infection (MOI). This ensures that each cell receives only one sgRNA, enabling accurate functional gene screening. In this article, we highlight the top three most popular libraries of the month and share key research papers to provide guidance, insights, and support for advancing your scientific studies. I. Sequential genome-wide CRISPR-Cas9 screens identify genes regulating cell-surface expression of tetraspanins Original Link: https://doi.org/10.1016/j.celrep.2023.112065 Four-transmembrane proteins belong to a superfamily of membrane proteins. They were first identified while searching for new cell surface antigens in mammalian cancer cells. Currently, 33 members of this four-trans...

  Prime editing is an improved gene editing technology based on the CRISPR/Cas system to achieve precise fragment insertion, deletion, and arbitrary substitution of bases at the target site of the genome, with higher accuracy and lower error rate. When it came out, it attracted widespread attention from many scientific researchers, and extensive research was conducted on the treatment of hereditary diseases, gene mutation diseases, and cancers. For example, correcting the mutant genes to treat genetic diseases or editing oncogenes in cancer cell genomes to prevent them from growing and spreading. The following three articles are about the clinical treatment of Prime Editing, bringing you the latest research trends.   Prime editing helps in the treatment of β - thalassemia, and no off-target  effect was detected         β - thalassemia is a hematopoietic system disease caused by a single gene mutation in the hemoglobin (HGB) subunit beta gene (HBB), res...