mProX™ Human GUCY2C Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- Kinase Cell Lines
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Published Data
Fig.1 Stimulation with KCl led to enhanced insulin release in MIN6c4 cells following Gucy2c depletion.
Although GSIS remained unaffected by Gucy2c knockdown, the cells in which Gucy2c was silenced displayed diminished insulin secretion compared to the control cells upon KCl stimulation.
Ref: Kobayashi, Masaki, et al. "Functional analysis of novel candidate regulators of insulin secretion in the MIN6 mouse pancreatic β cell line." PloS one 11.3 (2016): e0151927.
Pubmed: 26986842
DOI: 10.1371/journal.pone.0151927
Research Highlights
Rampuria, Pragya. et al. "Molecular insights into recognition of GUCY2C by T-cell engaging bispecific antibody anti-GUCY2CxCD3." Scientific reports, 2023.
The intestinal epithelial receptor Guanylyl Cyclase C (GUCY2C) has been identified as a potential target for colorectal cancer immunotherapy due to its presence as a cell surface antigen in various gastrointestinal malignancies. A recent advancement in this field is the development of a novel anti-GUCY2CxCD3 bispecific antibody (BsAb) that has entered clinical trials. To better understand the antibody's mechanism of action, researchers utilized a yeast surface-display approach and a peptide-based mapping strategy to identify the specific binding epitope on GUCY2C. It was determined that the N-terminal helix H2 of human GUCY2C is responsible for binding the antibody, and the crystal structure of this minimal epitope in complex with the anti-GUCY2C antibody domain was elucidated. Further investigation into the full-length extracellular domain (ECD) of GUCY2C revealed that the epitope is situated on the protruding membrane-distal helical region and plays a crucial role in the close spatial proximity of the two antigen arms of the BsAb, which is essential for its tumor killing activity.
Rampuria, Pragya. et al. "Molecular insights into recognition of GUCY2C by T-cell engaging bispecific antibody anti-GUCY2CxCD3." Scientific reports, 2023.
Pubmed:
37591971
DOI:
10.1038/s41598-023-40467-0
Yin, Lianhong. et al. "Single-cell analysis of cellular heterogeneity and interactions in the ischemia-reperfusion injured mouse intestine." Journal of pharmaceutical analysis, 2023.
In a study investigating the effects of intestinal ischemia,Äíreperfusion (II/R) injury in mice, researchers identified nine major cell populations out of 46,716 cells using single-cell RNA sequencing. Among these, 11 subclusters of enterocyte cells were discovered, including previously unknown enterocyte clusters 1 (EC1), 3 (EC3), and 8 (EC8) in the I 45 min/R 720 min group. EC1 and EC3 were found to play a role in digestion and absorption, while EC8 was involved in cell junctions. Additionally, TA cells at the stage of proliferation were identified after I 45 min/R 90 min and a resting state Paneth cluster 3 was observed in normal jejunum. Three new subsets of Paneth cells were discovered after I 45 min/R 90 min, with Paneth cluster 1 showing high antigen presentation activity. A novel subcluster of highly proliferative goblet cells (goblet cluster 5) was also discovered in this group. It was found that T cells, as a major part of the immune system, undergo changes during II/R injury. Interestingly, enterocyte cells were found to interact with stem cells, TA cells, Paneth cells, and goblet cells through the secretion of Guca2b and the Gucy2c receptor on cell membranes. Additionally, the enzyme glutathione S-transferase mu 3 (GSTM3) was identified as a marker that affects intestinal mucosal barrier function by regulating mitogen-activated protein kinase (MAPK) signaling during II/R injury. By uncovering the heterogeneity of intestinal cells, their communication, and the mechanism of GSTM3, this study provides a cellular basis for potential treatments of II/R injury.
Yin, Lianhong. et al. "Single-cell analysis of cellular heterogeneity and interactions in the ischemia-reperfusion injured mouse intestine." Journal of pharmaceutical analysis, 2023.
Pubmed:
37577387
DOI:
10.1016/j.jpha.2023.02.002