In Stock Cell Lines
The BCAP31 Knockout HK-2 Cell Line is a CRISPR/Cas9-edited human kidney proximal tubule epithelial cell line with disruption of BCAP31, an endoplasmic reticulum (ER) adaptor protein critical for ER-to-Golgi transport and ER-associated degradation (ERAD). BCAP31 interacts with BAP29, Derlin-1, and p97/VCP to regulate MHC class I trafficking and ER stress responses, modulating apoptosis via caspase-8/3 and CHOP. This knockout model enables investigation of ER stress biology, antigen presentation, and apoptosis in a renal epithelial context. Key applications include UPR marker profiling, ERAD functional assays, MHC-I surface expression analysis, and drug screening for ER stress modulators relevant to kidney disease, cancer immunotherapy, and neurodegenerative disorder research.
GPD1L Knockout HGC-27 Polyclonal Cells
Cat. No. ARG29848
AAR2 Knockout NCI-H1975 Polyclonal Cells
Cat. No. ARG30954
ALKBH1 Knockout HAP1 Polyclonal Cells
Cat. No. ARG34946
CASP3 Knockout HGC-27 Polyclonal Cells
Cat. No. ARG42441
ALG12 Knockout AGS Polyclonal Cells
Cat. No. ARG26536
Rat Renal Tubular Epithelial Cells
Cat. No. ARP0250
The BCAP31 Knockout HK-2 Cell Line is a CRISPR/Cas9-edited human kidney proximal tubule epithelial cell line with targeted disruption of the BCAP31 gene, which encodes the endoplasmic reticulum (ER) adaptor protein B-cell receptor-associated protein 31. This knockout model provides a defined loss-of-function system for studying BCAP31-dependent processes in ER protein quality control, antigen presentation, and stress signaling.
HK-2 is an immortalized proximal tubule epithelial line that retains critical renal functions, including nutrient and ion reabsorption, waste secretion, and acid-base balance maintenance. Widely used in renal physiology and toxicology, it offers a physiologically relevant epithelial context for investigating ER stress responses and immune interactions in the kidney.
BCAP31 resides in the ER membrane and facilitates anterograde transport of secretory and membrane proteins, including MHC class I, via a complex with BAP29 and Derlin-1. It is a component of the ER-associated degradation (ERAD) machinery, interacting with p97/VCP, HRD1 ubiquitin ligase, and the Sec61 translocon. BCAP31 activity is modulated by ER stress inducers (tunicamycin, thapsigargin) and UPR transcription factors ATF6 and XBP1s. Downstream, it regulates MHC-I surface expression, caspase-8/3 activation, and CHOP induction, integrating ER homeostasis with apoptosis and adaptive immunity.
In the HK-2 background, BCAP31 loss disrupts ER-to-Golgi transport and ERAD, causing misfolded protein accumulation and perturbed UPR signaling. This is particularly relevant to kidney pathophysiology, where ER stress contributes to acute kidney injury, nephrotoxicity, and diabetic nephropathy. Impaired MHC-I trafficking may reduce antigen presentation, providing a platform to study immune evasion and epithelial?CCD8+ T cell crosstalk. Altered caspase and Bcl-2 family regulation further enables dissection of ER stress-driven apoptotic pathways.
Researchers can utilize this knockout line for ER stress profiling via western blot of BiP, CHOP, and spliced XBP1, or RT-qPCR of UPR target genes. ERAD function can be assessed by co-immunoprecipitation of BCAP31 partners (Derlin-1, p97/VCP) and ERAD reporter assays. Flow cytometry quantifies MHC-I surface levels, while Annexin V and caspase activity assays measure apoptosis under tunicamycin or thapsigargin challenge. Additional applications include drug screening for ER stress modulators, cancer immunotherapy research, and renal disease modeling. For inquiries, contact Ascent Research.
