In Stock Cell Lines
Mus musculus (Mouse)
Ascites
Adherent
Bahcc1 Knockout RAW 264.7 Cell Line is a CRISPR/Cas9-edited murine macrophage line disrupted for Bahcc1, which encodes the chromatin-associated protein BAHCC1. BAHCC1 is regulated by TLR ligands and cytokines, interacts with Histone H3 and chromatin remodelers, and governs immune gene transcription. This model enables study of BAHCC1-dependent epigenetic control in macrophage activation and polarization. The RAW 264.7 macrophage background supports investigations into innate immune signaling and chromatin biology. Applications include ChIP-qPCR, RNA-seq, flow cytometry, and reporter assays to dissect BAHCC1??s roles in inflammatory disorders and hematological malignancy research.
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Bahcc1 Knockout RAW 264.7 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from Mus musculus RAW 264.7 macrophages. This gene-edited model features targeted disruption of the Bahcc1 gene, which encodes BAH and coiled-coil domain-containing protein 1, a putative chromatin-associated factor. The knockout cell line provides a loss-of-function system for investigating Bahcc1??s role in transcriptional regulation and epigenetic processes within an immune cell context.
RAW 264.7 is an Abelson murine leukemia virus-induced tumor-derived macrophage cell line widely used for studying monocytic/macrophage immune responses. These cells exhibit robust responsiveness to various immune stimuli and are a well-established model for macrophage activation, polarization, and signal transduction. The BALB/c-derived line retains many functional characteristics of primary macrophages, including phagocytic activity and inducible cytokine production, making it a suitable platform for genetic manipulation to dissect regulatory mechanisms in innate immunity.
BAHCC1 is predicted to function as a chromatin-associated protein that recognizes specific histone modifications, such as methylated Histone H3, through its BAH domain. Via its coiled-coil domain, it oligomerizes and integrates into chromatin remodeling complexes, thereby modulating access of transcriptional machinery to gene regulatory regions. In macrophages, BAHCC1 activity is regulated by upstream signals including Toll-like receptor (TLR) ligands, inflammatory cytokines, and cellular stress signals. Downstream, BAHCC1 influences the transcription of cytokine genes and broader immune response programs. It interacts with core histones, chromatin remodelers, and transcription factors, positioning it within pathways that convert extrinsic stimuli into epigenetic changes controlling gene expression.
In RAW 264.7 cells, BAHCC1 is implicated in coordinating macrophage activation and polarization decisions by linking signal-responsive chromatin dynamics to transcriptional outputs. The knockout model thus allows dissection of how BAHCC1-dependent epigenetic regulation shapes macrophage phenotype during responses to pro-inflammatory or anti-inflammatory cues. Its disruption may alter the expression kinetics of key cytokines and activation markers, providing insight into macrophage plasticity and the epigenetic gating of immune gene loci.
The Bahcc1 Knockout RAW 264.7 Cell Line is a valuable tool for functional genomics screens, targeted epigenetic studies, and macrophage biology research. Researchers can employ chromatin immunoprecipitation coupled with quantitative PCR (ChIP-qPCR) to map histone modification changes at immunoregulatory loci, RNA sequencing (RNA-seq) for transcriptome-wide dissection of BAHCC1-regulated gene networks, and western blotting to verify candidate protein expression changes. Flow cytometry enables profiling of macrophage surface markers and activation states, while luciferase reporter assays offer quantitative measurement of transcription factor activity downstream of BAHCC1. These applications support investigations into hematological malignancies linked to chromatin dysregulation and inflammatory disorders where macrophage responses are pivotal. For detailed information on validation and availability, please contact Ascent Research.