In Stock Cell Lines
Homo sapiens (Human)
Skin
Adherent
The SMPD3 Knockout HaCat Cell Line is a CRISPR/Cas9-edited knockout cell line in which the SMPD3 gene has been disrupted in the HaCat human keratinocyte line. SMPD3 encodes neutral sphingomyelinase 2 (nSMase2), which hydrolyzes sphingomyelin to ceramide, a lipid mediator that regulates apoptosis, differentiation, and stress responses downstream of TNF-alpha and p53. This model enables controlled studies of ceramide signaling and its role in epidermal biology. With applications in skin disease modeling, drug screening, and barrier function analysis, the cell line supports techniques such as ceramide quantification, annexin V assays, and western blotting for nSMase2 and targets including caspase-3 and JNK. It is a valuable resource for investigating sphingolipid-related pathologies. Contact Ascent Research for details.
MTSS1 Knockout NCI-H1975 Polyclonal Cells
Cat. No. ARG16532
GAS2L1 Knockout NCI-H1299 Polyclonal Cells
Cat. No. ARG17508
MAN2A2 Knockout jurkat Polyclonal Cells
Cat. No. ARG12856
DFFB Knockout Hela Polyclonal Cells
Cat. No. ARG7940
KCNJ15 Knockout HAP1 Polyclonal Cells
Cat. No. ARG22943
DNAJC1 Knockout NCI-H1975 Polyclonal Cells
Cat. No. ARG39173
The SMPD3 Knockout HaCat Cell Line is a CRISPR/Cas9-edited knockout cell line with targeted disruption of the SMPD3 gene in HaCat human keratinocytes. This loss-of-function model is designed for investigating neutral sphingomyelinase 2 (nSMase2) function in skin biology and disease.
HaCat cells are a spontaneously immortalized human keratinocyte line widely used for studying epidermal differentiation, barrier function, and skin pathologies. Their stable phenotype and ease of culture make them a preferred host for genetic perturbations, and the SMPD3 knockout provides a reproducible system to examine sphingolipid signaling in keratinocytes.
SMPD3 encodes neutral sphingomyelinase 2 (nSMase2), a membrane-associated phosphodiesterase that hydrolyzes sphingomyelin into the bioactive lipid ceramide and phosphocholine. This enzymatic step is a central hub in sphingolipid metabolism, linking extracellular stimuli such as TNF-alpha, UV radiation, oxidative stress, and p53 activation to intracellular ceramide-mediated signaling. nSMase2 physically interacts with the TNF receptor and FAN to relay apoptotic signals, and its product ceramide directly promotes activation of caspase-3 and JNK while also modulating NF-kB and p38 MAPK pathways. Disruption of SMPD3 therefore eliminates nSMase2 activity, blocking stress-induced ceramide generation and attenuating downstream pro-apoptotic and inflammatory programs.
In human epidermal keratinocytes, nSMase2-derived ceramide is indispensable for programmed differentiation, cornified envelope formation, and maintenance of the skin barrier. Loss of SMPD3 in HaCat cells impedes ceramide-driven differentiation and confers resistance to ceramide-dependent apoptosis, replicating features observed in disorders characterized by impaired barrier function, such as atopic dermatitis and psoriasis. This knockout thus serves as a relevant cellular model to dissect how aberrant sphingolipid metabolism drives keratinocyte dysfunction, hyperproliferation, and inflammation, and to test therapeutic interventions targeting these pathways.
The SMPD3 Knockout HaCat Cell Line supports a diverse array of applications including ceramide quantification, annexin V apoptosis assays, western blot analysis of nSMase2, caspase-3, JNK, and NF-kB, immunofluorescence for differentiation markers, and RT-qPCR. It is suitable for drug screening, transwell barrier function tests, and integration into 3D skin equivalents. For detailed technical specifications and ordering information, please contact Ascent Research.
