In Stock Cell Lines
Homo sapiens (Human)
Blood (peripheral blood)
Suspension
The HDAC1 Knockout Jurkat Cell Line is a CRISPR/Cas9-edited knockout model derived from Jurkat human T lymphocyte leukemia cells. It enables loss-of-function studies of histone deacetylase 1, a transcriptional repressor that operates within SIN3A, NuRD, and CoREST corepressor complexes and regulates key targets such as p21 and c-Myc. By disrupting HDAC1-mediated chromatin remodeling, this model aids in investigating T cell signaling, apoptosis, and leukemia biology. It is suitable for applications including drug screening, epigenetic profiling, and functional genomics assays such as western blotting, RT-qPCR, and flow cytometry.
CAMK2A Knockout CaSki Polyclonal Cells
Cat. No. ARG35448
GMPPA Knockout SK-HEP-1 Polyclonal Cells
Cat. No. ARG15602
ARL3 Knockout NCI-H1975 Polyclonal Cells
Cat. No. ARG31224
DST Knockout huh-7 Polyclonal Cells
Cat. No. ARG39858
MCAM Knockout MES-OV Polyclonal Cells
Cat. No. ARG6788
PAGR1 Knockout 786-O Polyclonal Cells
Cat. No. ARG4649
The HDAC1 Knockout Jurkat Cell Line is a CRISPR/Cas9-edited knockout cell line providing a loss-of-function model for studying histone deacetylase 1 (HDAC1). Derived via CRISPR/Cas9-mediated gene disruption, this product enables investigation of HDAC1’s role in transcriptional regulation and chromatin remodeling. It is a valuable resource for functional genomics and epigenetics research.
The host Jurkat cell line is an immortalized human T lymphocyte line established from acute T cell leukemia. Widely employed as a model for T cell signaling and apoptosis, Jurkat cells exhibit well-characterized pathways relevant to leukemia biology and immunology. Their robust proliferation and genetic tractability make them ideal for knockout studies.
HDAC1 is a class I histone deacetylase that removes acetyl groups from histones, promoting chromatin compaction and transcriptional repression. It operates within corepressor complexes such as SIN3A, NuRD, and CoREST, interacting with scaffold proteins RbAp46/RbAp48 and MTA1/2. Upstream regulators including CK2 kinase and p53 modulate HDAC1 activity. HDAC1 transcriptionally represses targets like p21 (CDKN1A), c-Myc, E2F target genes, and pro-apoptotic factors, thereby controlling cell cycle progression and apoptosis. In Notch signaling, HDAC1 forms repressive complexes with NICD, CSL, and MAML1, counteracting co-activators like p300/CBP. This integration of signals from Wnt, TGF-beta, and p53 pathways underscores HDAC1’s role in coordinating gene expression.
In Jurkat T leukemia cells, HDAC1-mediated suppression of tumor suppressors and apoptotic genes contributes to oncogenic transformation. Knockout of HDAC1 disrupts these repressive mechanisms, leading to altered expression of p21, c-Myc, and pro-apoptotic targets. This cell line thus provides a relevant model for dissecting epigenetic drivers of T cell leukemia and lymphoma. It enables investigation of how HDAC1 loss impacts cell cycle checkpoints and apoptotic signaling in a malignant background.
This knockout cell line is suited for diverse assays including western blotting for HDAC1 and acetyl-histone levels, RT-qPCR for target gene expression, ChIP-qPCR for histone modification mapping, and flow cytometry for apoptosis and proliferation analyses. Applications span drug sensitivity screening, functional genomics, and mechanistic studies of T cell signaling. For further information, contact Ascent Research.
