Description

The LOC102549962 Knockout H9C2 Cell Line is a CRISPR/Cas9-edited knockout cell line designed for loss-of-function studies of the rat long non-coding RNA LOC102549962 in a cardiac muscle context. This product provides a genetically disrupted model in which the target gene has been inactivated using CRISPR/Cas9-mediated gene disruption, enabling researchers to dissect the regulatory roles of this lncRNA in cardiomyoblast biology. The knockout cell line is supplied as a stable adherent culture derived from the H9C2 host background and is suitable for a broad range of molecular and cellular analyses relevant to cardiovascular research.

The parental H9C2 cell line is a subclone of the H9(2-1) line, originally isolated from embryonic BDIX rat heart ventricular tissue. H9C2 cells are a well-established model cardiomyoblast line that retains characteristics of embryonic heart cells, including expression of cardiac transcription factors, ion channels, and contractile proteins. This background provides a physiologically relevant host for investigating the effects of LOC102549962 knockout on cardiomyocyte differentiation, electrophysiology, and hypertrophic responses, reflecting the cellular context of developing and stressed cardiac muscle.

LOC102549962 encodes a regulatory long non-coding RNA that functions as a scaffold for chromatin-modifying complexes, interacting directly with PRC2 components, LSD1, EZH2, and DNMT1 to modulate gene expression. It is positioned within key cardiac signaling networks, receiving upstream activation from Wnt ligands, TGF-beta, and Hippo pathway effectors YAP and TAZ, while transcriptionally regulating downstream targets such as MYH6, MYH7, ACTC1, KCNA5, and SCN5A. The lncRNA also interacts with microRNAs miR-1 and miR-133 and transcription factors MEF2C, GATA4, NKX2-5, and TBX5, forming a regulatory hub that influences cardiomyoblast function and cardiac muscle contraction.

Disruption of LOC102549962 in H9C2 cells is expected to perturb these interconnected regulatory networks, providing a powerful model to study the molecular basis of cardiac hypertrophy and heart failure. The knockout may alter SMAD2/3-SMAD4 signaling downstream of TGF-beta, beta-catenin activity in the Wnt pathway, and YAP/TAZ-mediated transcriptional programs, thereby affecting cardiomyocyte growth and electrophysiological properties. This system enables precise investigation of lncRNA-dependent gene regulation in a cell line that mirrors embryonic cardiac phenotypes, making it valuable for dissecting both developmental and pathological mechanisms.

This cell line is optimized for a variety of research applications, including transcriptomic profiling via RNA-seq, validation of gene expression changes by RT-qPCR and Western blotting, and cellular hypertrophy assays using angiotensin II stimulation. It supports functional studies of lncRNA-chromatin interactions through ChIRP and RIP, immunofluorescence for cardiac markers, and electrophysiological recordings for ion channel analysis. Additionally, the model is suitable for drug screening targeting cardiac diseases such as myocardial infarction and congenital heart disease. For further information, please contact Ascent Research.