In Stock Cell Lines
Mus musculus (Mouse)
Muscle (skeletal muscle)
Adherent
The Mef2d Knockout C2C12 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from C2C12 mouse myoblasts. This loss-of-function model targets the transcription factor MEF2D, which collaborates with MyoD and myogenin to drive muscle-specific gene expression. MEF2D is activated by p38 MAPK and inhibited through interaction with class IIa HDACs, such as HDAC4. Researchers can study myogenic differentiation, transcriptional control, and HDAC-mediated repression. Typical assays include myotube fusion analysis, MyHC immunostaining, co-immunoprecipitation, and luciferase reporter assays, with applications in muscle atrophy and drug screening. Contact Ascent Research for technical support.
PARVB Knockout NCI-H1975 Polyclonal Cells
Cat. No. ARG16397
NRG4 Knockout SK-Hep-1 Polyclonal Cells
Cat. No. ARG15345
GATA6 Knockout A549 Polyclonal Cells
Cat. No. ARG10499
ID3 Knockout HT29 Polyclonal Cells
Cat. No. ARG36178
CCDC167 Knockout NCI-H1975 Polyclonal Cells
Cat. No. ARG42977
HS-SY-II
Cat. No. ARC0323
The Mef2d Knockout C2C12 Cell Line is a CRISPR/Cas9-edited knockout cell line targeting the Mef2d gene in the C2C12 mouse myoblast background. This stable loss-of-function model enables dissection of MEF2D??s role in transcriptional regulation of skeletal myogenesis. By eliminating endogenous MEF2D, researchers can investigate gene activation, cell differentiation, and cross-talk with myogenic regulatory factors without residual wild-type interference. The line is provided as a validated knockout cell line ready for downstream assays.
The parental C2C12 cell line, a subclone of the C2 myoblast line from C3H mouse satellite cells, is a classic in vitro model for muscle differentiation. Upon serum withdrawal, these myoblasts fuse into multinucleated myotubes, recapitulating myogenesis. This synchronized differentiation capacity makes C2C12 an ideal host for examining transcription factors like MEF2D and their temporal regulation of muscle genes such as MyoD and myogenin.
MEF2D is a MADS-box transcription factor that binds MEF2 response elements and cooperates with MyoD and myogenin to activate muscle-specific genes including MCK, MHC isoforms, and desmin, as well as miR-1 and miR-133. Its activity is enhanced by p38 MAPK-mediated phosphorylation and calcium/calcineurin-dependent NFAT nuclear translocation. Conversely, class IIa HDACs like HDAC4 bind MEF2D and recruit repressive complexes. MEF2D also interacts with p300/CBP coactivators and integrates signals from PI3K/AKT and ERK5 pathways, positioning it as a central node in myogenic signaling.
In C2C12 cells, MEF2D is critical for terminal differentiation; its loss impairs myotube formation and reduces expression of late myogenic markers. The knockout cell line thus enables rigorous functional analysis of MEF2D-dependent transcriptional programs and HDAC-mediated repression. Although derived from muscle precursors, the model also informs signaling relevant to cardiac hypertrophy and neurodegeneration, as MEF2D regulates cell survival genes such as Bcl-2 family members and Nur77 across tissues.
The line supports diverse assays: RT-qPCR and Western blotting for target validation, myotube fusion index and MyHC immunostaining for differentiation assessment, luciferase reporters for MEF2-element activity, co-immunoprecipitation for protein interactions, and ChIP-qPCR for genomic binding. It is applicable in muscle atrophy models and compound screening for muscle-wasting diseases. Researchers can leverage the Mef2d Knockout C2C12 Cell Line for fundamental myogenesis studies and translational research. For technical details, please contact Ascent Research.
