In Stock Cell Lines
Mus musculus (Mouse)
Brain (hippocampus)
Adherent
The Nucks1 Knockout HT22 Cell Line is a CRISPR/Cas9-edited knockout cell line featuring disruption of the Nucks1 gene in the mouse hippocampal HT22 neuronal model. Nucks1, a CK2/CDK-phosphorylated nuclear protein, regulates DNA repair and transcription of SNCA (alpha-synuclein), p21, and BAX. This knockout impairs DNA damage response and reduces alpha-synuclein expression, making it ideal for studying Parkinson??s disease and neuronal stress pathways. Applications include oxidative stress assays, DNA damage analysis, and apoptosis studies using Western blotting, RT-qPCR, and flow cytometry. The HT22 background provides a well-established system for investigating glutamate toxicity and neurodegeneration mechanisms.
AIMP1 Knockout MES-OV Polyclonal Cells
Cat. No. ARG24089
IDH3G Knockout 786-O Polyclonal Cells
Cat. No. ARG25314
KPNA1 Knockout A2780 Polyclonal Cells
Cat. No. ARG29334
ABHD6 Knockout NCI-H1975 Polyclonal Cells
Cat. No. ARG30973
HCC1937 eGFP-Luc Stable Cell Line
Cat. No. ARG0259
Human Articular Chondrocytes
Cat. No. ARP0156
The Nucks1 Knockout HT22 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from the mouse hippocampal neuronal HT22 cell line, in which the Nucks1 gene has been disrupted. This loss-of-function model enables investigation of Nucks1-dependent cellular processes, including DNA repair, cell cycle regulation, and transcriptional control. The knockout cell line provides a defined genetic background for studying the role of Nucks1 in neuronal stress responses and neurodegenerative pathways.
HT22 is an immortalized mouse hippocampal neuronal cell line, originally a subclone of HT4, widely employed as a model for neuronal oxidative stress and glutamate-induced toxicity. HT22 cells lack functional ionotropic glutamate receptors, undergoing oxidative glutamate toxicity via cystine/glutamate antiporter inhibition, which mimics excitotoxicity-independent neuronal death. This makes HT22 particularly valuable for studying neurodegeneration mechanisms mediated by oxidative stress, a key feature in Parkinson??s disease and other disorders.
Nucks1 (Nuclear Casein Kinase and Cyclin-Dependent Kinase Substrate 1) is a nuclear phosphoprotein that functions at the intersection of DNA damage response and transcriptional regulation. It is phosphorylated by CK2 and CDKs (CDK1, CDK2) upon DNA damage, acting downstream of ATM/ATR signaling. Nucks1 transcriptionally regulates the alpha-synuclein gene SNCA, a central player in Parkinson??s disease pathology, as well as cell cycle and apoptosis genes such as CDKN1A (p21) and BAX. Through these interactions, Nucks1 modulates cell cycle checkpoint control and apoptosis in response to genotoxic stress.
In the HT22 neuronal background, Nucks1 knockout significantly alters cellular responses to oxidative and genotoxic insults. The loss of Nucks1 impairs DNA damage repair and cell cycle checkpoint activation, while reducing SNCA expression, which may influence alpha-synuclein aggregation dynamics. This model thus recapitulates molecular alterations observed in Parkinson??s disease and other neurodegenerative conditions, offering a platform to dissect how Nucks1-dependent pathways affect neuronal vulnerability to stress.
Applications include neurodegenerative disease research, DNA damage response studies, and apoptosis assays. Researchers can employ Western blotting, RT-qPCR, and immunofluorescence to quantify changes in SNCA, p21, BAX, and phospho-ATM/ATR. Flow cytometry enables cell cycle profiling and apoptosis detection, while the comet assay measures DNA damage accumulation. Glutamate-induced oxidative stress assays using this knockout line reveal the role of Nucks1 in neuronal survival. For further information or technical support, please contact Ascent Research.
