In Stock Cell Lines
Mus musculus (Mouse)
Bone (calvaria)
Adherent
The Ccdc134 Knockout MC3T3-E1 Cell Line is a CRISPR/Cas9-edited Mus musculus preosteoblast cell line with targeted disruption of the Ccdc134 gene. This model leverages the MC3T3-E1 host, a calvaria-derived line capable of osteogenic differentiation and mineralization, to study CCDC134 function in bone cell biology. CCDC134 acts as a transcriptional co-regulator in the p53 pathway, interacting with p53 and modulating downstream targets such as CDKN1A and BAX in response to DNA damage. The knockout line is suitable for investigating osteoblast differentiation, DNA damage repair, apoptosis, and bone metastasis, employing assays like Alizarin Red staining, flow cytometry, and gene expression analysis.
ERI3 Knockout Hela Polyclonal Cells
Cat. No. ARG8856
IL17RA Knockout MES-OV Polyclonal Cells
Cat. No. ARG24623
ADNP2 Knockout HEK293T Polyclonal Cells
Cat. No. ARG25615
DNPEP Knockout HGC-27 Polyclonal Cells
Cat. No. ARG39470
Mouse Gallbladder Epithelial Cell Medium
Cat. No. ARM0473
NCI-H647
Cat. No. ARC0647
The Ccdc134 Knockout MC3T3-E1 Cell Line is a CRISPR/Cas9-mediated gene disruption model targeting the Ccdc134 gene in the Mus musculus MC3T3-E1 preosteoblast cell line. This engineered cell line provides a stable loss-of-function platform to investigate the molecular functions of the CCDC134 protein. The knockout is generated through CRISPR/Cas9 technology, effectively disrupting the endogenous Ccdc134 locus to abolish protein expression, enabling precise dissection of the gene’s role in cellular processes.
The MC3T3-E1 host cell line is a well-established preosteoblastic model derived from C57BL/6 mouse calvaria. This subclone is distinguished by its high osteogenic differentiation potential and capacity for extracellular matrix mineralization in vitro, making it a cornerstone for studying osteoblast biology. Under appropriate induction conditions, MC3T3-E1 cells progress through differentiation stages, recapitulating key events of bone formation, and thus serve as a physiologically relevant system for exploring gene function during osteogenesis.
CCDC134, a coiled-coil domain-containing protein, is implicated in the cellular response to DNA damage, functioning as a putative transcriptional co-regulator within the p53 signaling pathway. Upon genotoxic stress, p53 activates a transcriptional program that includes CDKN1A (p21) for cell cycle arrest and BAX for apoptosis. CCDC134 interacts with p53 and is thought to modulate the expression of these downstream targets, thereby influencing cell cycle progression and survival. Upstream activation by DNA damage stimuli positions CCDC134 at the intersection of genome stability and cell fate decisions, with potential involvement in tumor suppression mechanisms.
In the context of MC3T3-E1 preosteoblasts, knockout of Ccdc134 offers a unique model to interrogate DNA damage response pathways during osteogenic differentiation. Since these cells are capable of mineralization and osteoblastic maturation, loss of CCDC134 may alter the balance between proliferation arrest and apoptosis when differentiation is coupled with genotoxic challenges. This model thus facilitates studies on how DNA repair and cell cycle checkpoints are integrated with lineage-specific differentiation programs in bone-forming cells, with implications for understanding bone diseases and cancer metastasis to bone.
Researchers can employ this Ccdc134 knockout cell line in a broad range of assays, including western blotting and RT-qPCR for gene expression analysis, Alizarin Red S staining to monitor osteogenic differentiation, MTT assays for proliferation, and flow cytometry for cell cycle and apoptosis (Annexin V) profiling. Following DNA damage induction by ??-irradiation, the line enables detailed investigation of p53-mediated responses. Applications include osteosarcoma research, studies of DNA repair in bone biology, and bone metastasis models. For further information, please contact Ascent Research.
