Source 1primary paper2019Small GTPases
Toolkit/single cell-based analysis
single cell-based analysis
Taxonomy: Technique Branch / Method. Workflows sit above the mechanism and technique branches rather than replacing them.
Summary
Single cell-based analysis is a quantitative cellular assay framework developed to compare the activities of overexpressed full-length guanine nucleotide exchange factors in primary human endothelial cells. It was applied with single-cell FRET Rho GTPase biosensors to measure GEF-driven activation of Cdc42 and Rac1.
Usefulness & Problems
Why this is useful
This framework enables quantitative comparison of GEF efficiency at single-cell resolution in a primary endothelial cell context. In the cited study, it supported ranking endothelial GEFs for their ability to activate Cdc42 and assessing selectivity relative to Rac1.
Problem solved
The method addresses the problem of comparing the cellular activities of multiple overexpressed full-length GEFs in a quantitative manner. It also helps identify endothelial GEFs that may directly or indirectly activate Cdc42 using single-cell biosensor readouts.
Problem links
A single-cell analysis method is plausibly relevant because the gap centers on heterogeneous cellular states that are obscured in bulk measurements. The summary supports quantitative comparison of cellular activities at single-cell resolution, though not true multimodal integration.
Taxonomy & Function
Primary hierarchy
Technique Branch
Method: A concrete computational method used to design, rank, or analyze an engineered system.
Mechanisms
fret-based biosensingfret-based biosensingsingle-cell quantitative activity measurementsingle-cell quantitative activity measurementTarget processes
No target processes tagged yet.
Implementation Constraints
cofactor dependency: cofactor requirement unknownencoding mode: genetically encodedimplementation constraint: context specific validationoperating role: builder
The reported implementation used single-cell FRET measurements with Rho GTPase biosensors in primary human endothelial cells. The assay compared overexpressed full-length GEF constructs, but the supplied evidence does not specify biosensor design, fluorophores, imaging hardware, or analysis pipeline details.
The supplied evidence describes application in one published study in primary human endothelial cells and does not establish performance across other cell types or signaling systems. The evidence also does not report throughput, sensitivity limits, statistical robustness, or independent replication.
Validation
Cell-freeBacteriaMammalianMouseHumanTherapeuticIndep. Replication
Supporting Sources
Ranked Claims
PLEKHG2, FGD1, PLEKHG1, and PREX1 induced the most efficient Cdc42 activation among the tested endothelial GEFs, and FGD1 showed the highest selectivity.
Our data reveal GEF dependent activation of Cdc42, with the most efficient Cdc42 activation induced by PLEKHG2, FGD1, PLEKHG1 and PREX1 and the highest selectivity for FGD1.
PLEKHG2, FGD1, PLEKHG1, and PREX1 induced the most efficient Cdc42 activation among the tested endothelial GEFs, and FGD1 showed the highest selectivity.
Our data reveal GEF dependent activation of Cdc42, with the most efficient Cdc42 activation induced by PLEKHG2, FGD1, PLEKHG1 and PREX1 and the highest selectivity for FGD1.
PLEKHG2, FGD1, PLEKHG1, and PREX1 induced the most efficient Cdc42 activation among the tested endothelial GEFs, and FGD1 showed the highest selectivity.
Our data reveal GEF dependent activation of Cdc42, with the most efficient Cdc42 activation induced by PLEKHG2, FGD1, PLEKHG1 and PREX1 and the highest selectivity for FGD1.
PLEKHG2, FGD1, PLEKHG1, and PREX1 induced the most efficient Cdc42 activation among the tested endothelial GEFs, and FGD1 showed the highest selectivity.
Our data reveal GEF dependent activation of Cdc42, with the most efficient Cdc42 activation induced by PLEKHG2, FGD1, PLEKHG1 and PREX1 and the highest selectivity for FGD1.
PLEKHG2, FGD1, PLEKHG1, and PREX1 induced the most efficient Cdc42 activation among the tested endothelial GEFs, and FGD1 showed the highest selectivity.
Our data reveal GEF dependent activation of Cdc42, with the most efficient Cdc42 activation induced by PLEKHG2, FGD1, PLEKHG1 and PREX1 and the highest selectivity for FGD1.
PLEKHG2, FGD1, PLEKHG1, and PREX1 induced the most efficient Cdc42 activation among the tested endothelial GEFs, and FGD1 showed the highest selectivity.
Our data reveal GEF dependent activation of Cdc42, with the most efficient Cdc42 activation induced by PLEKHG2, FGD1, PLEKHG1 and PREX1 and the highest selectivity for FGD1.
PLEKHG2, FGD1, PLEKHG1, and PREX1 induced the most efficient Cdc42 activation among the tested endothelial GEFs, and FGD1 showed the highest selectivity.
Our data reveal GEF dependent activation of Cdc42, with the most efficient Cdc42 activation induced by PLEKHG2, FGD1, PLEKHG1 and PREX1 and the highest selectivity for FGD1.
PLEKHG2, FGD1, PLEKHG1, and PREX1 induced the most efficient Cdc42 activation among the tested endothelial GEFs, and FGD1 showed the highest selectivity.
Our data reveal GEF dependent activation of Cdc42, with the most efficient Cdc42 activation induced by PLEKHG2, FGD1, PLEKHG1 and PREX1 and the highest selectivity for FGD1.
PLEKHG2, FGD1, PLEKHG1, and PREX1 induced the most efficient Cdc42 activation among the tested endothelial GEFs, and FGD1 showed the highest selectivity.
Our data reveal GEF dependent activation of Cdc42, with the most efficient Cdc42 activation induced by PLEKHG2, FGD1, PLEKHG1 and PREX1 and the highest selectivity for FGD1.
PLEKHG2, FGD1, PLEKHG1, and PREX1 induced the most efficient Cdc42 activation among the tested endothelial GEFs, and FGD1 showed the highest selectivity.
Our data reveal GEF dependent activation of Cdc42, with the most efficient Cdc42 activation induced by PLEKHG2, FGD1, PLEKHG1 and PREX1 and the highest selectivity for FGD1.
Single cell FRET measurements with Rho GTPase biosensors were used in primary human endothelial cells to monitor GEF efficiency toward Cdc42 and Rac1.
By performing single cell FRET measurements with Rho GTPase biosensors in primary human ECs, we monitored GEF efficiency towards Cdc42 and Rac1.
Single cell FRET measurements with Rho GTPase biosensors were used in primary human endothelial cells to monitor GEF efficiency toward Cdc42 and Rac1.
By performing single cell FRET measurements with Rho GTPase biosensors in primary human ECs, we monitored GEF efficiency towards Cdc42 and Rac1.
Single cell FRET measurements with Rho GTPase biosensors were used in primary human endothelial cells to monitor GEF efficiency toward Cdc42 and Rac1.
By performing single cell FRET measurements with Rho GTPase biosensors in primary human ECs, we monitored GEF efficiency towards Cdc42 and Rac1.
Single cell FRET measurements with Rho GTPase biosensors were used in primary human endothelial cells to monitor GEF efficiency toward Cdc42 and Rac1.
By performing single cell FRET measurements with Rho GTPase biosensors in primary human ECs, we monitored GEF efficiency towards Cdc42 and Rac1.
Single cell FRET measurements with Rho GTPase biosensors were used in primary human endothelial cells to monitor GEF efficiency toward Cdc42 and Rac1.
By performing single cell FRET measurements with Rho GTPase biosensors in primary human ECs, we monitored GEF efficiency towards Cdc42 and Rac1.
Single cell FRET measurements with Rho GTPase biosensors were used in primary human endothelial cells to monitor GEF efficiency toward Cdc42 and Rac1.
By performing single cell FRET measurements with Rho GTPase biosensors in primary human ECs, we monitored GEF efficiency towards Cdc42 and Rac1.
Single cell FRET measurements with Rho GTPase biosensors were used in primary human endothelial cells to monitor GEF efficiency toward Cdc42 and Rac1.
By performing single cell FRET measurements with Rho GTPase biosensors in primary human ECs, we monitored GEF efficiency towards Cdc42 and Rac1.
Single cell FRET measurements with Rho GTPase biosensors were used in primary human endothelial cells to monitor GEF efficiency toward Cdc42 and Rac1.
By performing single cell FRET measurements with Rho GTPase biosensors in primary human ECs, we monitored GEF efficiency towards Cdc42 and Rac1.
Single cell FRET measurements with Rho GTPase biosensors were used in primary human endothelial cells to monitor GEF efficiency toward Cdc42 and Rac1.
By performing single cell FRET measurements with Rho GTPase biosensors in primary human ECs, we monitored GEF efficiency towards Cdc42 and Rac1.
Single cell FRET measurements with Rho GTPase biosensors were used in primary human endothelial cells to monitor GEF efficiency toward Cdc42 and Rac1.
By performing single cell FRET measurements with Rho GTPase biosensors in primary human ECs, we monitored GEF efficiency towards Cdc42 and Rac1.
The study characterized endothelial GEFs that may directly or indirectly activate Cdc42.
Together, our study characterized endothelial GEFs that may directly or indirectly activate Cdc42
The study characterized endothelial GEFs that may directly or indirectly activate Cdc42.
Together, our study characterized endothelial GEFs that may directly or indirectly activate Cdc42
The study characterized endothelial GEFs that may directly or indirectly activate Cdc42.
Together, our study characterized endothelial GEFs that may directly or indirectly activate Cdc42
The study characterized endothelial GEFs that may directly or indirectly activate Cdc42.
Together, our study characterized endothelial GEFs that may directly or indirectly activate Cdc42
The study characterized endothelial GEFs that may directly or indirectly activate Cdc42.
Together, our study characterized endothelial GEFs that may directly or indirectly activate Cdc42
The study characterized endothelial GEFs that may directly or indirectly activate Cdc42.
Together, our study characterized endothelial GEFs that may directly or indirectly activate Cdc42
The study characterized endothelial GEFs that may directly or indirectly activate Cdc42.
Together, our study characterized endothelial GEFs that may directly or indirectly activate Cdc42
The study characterized endothelial GEFs that may directly or indirectly activate Cdc42.
Together, our study characterized endothelial GEFs that may directly or indirectly activate Cdc42
The study characterized endothelial GEFs that may directly or indirectly activate Cdc42.
Together, our study characterized endothelial GEFs that may directly or indirectly activate Cdc42
The study characterized endothelial GEFs that may directly or indirectly activate Cdc42.
Together, our study characterized endothelial GEFs that may directly or indirectly activate Cdc42
A new single cell-based analysis was developed to enable quantitative comparison of cellular activities of overexpressed full-length GEFs.
A new, single cell-based analysis was developed and used to enable the quantitative comparison of cellular activities of the overexpressed full-length GEFs.
A new single cell-based analysis was developed to enable quantitative comparison of cellular activities of overexpressed full-length GEFs.
A new, single cell-based analysis was developed and used to enable the quantitative comparison of cellular activities of the overexpressed full-length GEFs.
A new single cell-based analysis was developed to enable quantitative comparison of cellular activities of overexpressed full-length GEFs.
A new, single cell-based analysis was developed and used to enable the quantitative comparison of cellular activities of the overexpressed full-length GEFs.
A new single cell-based analysis was developed to enable quantitative comparison of cellular activities of overexpressed full-length GEFs.
A new, single cell-based analysis was developed and used to enable the quantitative comparison of cellular activities of the overexpressed full-length GEFs.
A new single cell-based analysis was developed to enable quantitative comparison of cellular activities of overexpressed full-length GEFs.
A new, single cell-based analysis was developed and used to enable the quantitative comparison of cellular activities of the overexpressed full-length GEFs.
A new single cell-based analysis was developed to enable quantitative comparison of cellular activities of overexpressed full-length GEFs.
A new, single cell-based analysis was developed and used to enable the quantitative comparison of cellular activities of the overexpressed full-length GEFs.
A new single cell-based analysis was developed to enable quantitative comparison of cellular activities of overexpressed full-length GEFs.
A new, single cell-based analysis was developed and used to enable the quantitative comparison of cellular activities of the overexpressed full-length GEFs.
A new single cell-based analysis was developed to enable quantitative comparison of cellular activities of overexpressed full-length GEFs.
A new, single cell-based analysis was developed and used to enable the quantitative comparison of cellular activities of the overexpressed full-length GEFs.
A new single cell-based analysis was developed to enable quantitative comparison of cellular activities of overexpressed full-length GEFs.
A new, single cell-based analysis was developed and used to enable the quantitative comparison of cellular activities of the overexpressed full-length GEFs.
A new single cell-based analysis was developed to enable quantitative comparison of cellular activities of overexpressed full-length GEFs.
A new, single cell-based analysis was developed and used to enable the quantitative comparison of cellular activities of the overexpressed full-length GEFs.
A new single cell-based analysis was developed to enable quantitative comparison of cellular activities of overexpressed full-length GEFs.
A new, single cell-based analysis was developed and used to enable the quantitative comparison of cellular activities of the overexpressed full-length GEFs.
A new single cell-based analysis was developed to enable quantitative comparison of cellular activities of overexpressed full-length GEFs.
A new, single cell-based analysis was developed and used to enable the quantitative comparison of cellular activities of the overexpressed full-length GEFs.
A new single cell-based analysis was developed to enable quantitative comparison of cellular activities of overexpressed full-length GEFs.
A new, single cell-based analysis was developed and used to enable the quantitative comparison of cellular activities of the overexpressed full-length GEFs.
A new single cell-based analysis was developed to enable quantitative comparison of cellular activities of overexpressed full-length GEFs.
A new, single cell-based analysis was developed and used to enable the quantitative comparison of cellular activities of the overexpressed full-length GEFs.
A new single cell-based analysis was developed to enable quantitative comparison of cellular activities of overexpressed full-length GEFs.
A new, single cell-based analysis was developed and used to enable the quantitative comparison of cellular activities of the overexpressed full-length GEFs.
A new single cell-based analysis was developed to enable quantitative comparison of cellular activities of overexpressed full-length GEFs.
A new, single cell-based analysis was developed and used to enable the quantitative comparison of cellular activities of the overexpressed full-length GEFs.
A new single cell-based analysis was developed to enable quantitative comparison of cellular activities of overexpressed full-length GEFs.
A new, single cell-based analysis was developed and used to enable the quantitative comparison of cellular activities of the overexpressed full-length GEFs.
Approval Evidence
1 source1 linked approval claimfirst-pass slug single-cell-based-analysis
A new, single cell-based analysis was developed and used to enable the quantitative comparison of cellular activities of the overexpressed full-length GEFs.
Source:
method developmentsupports
A new single cell-based analysis was developed to enable quantitative comparison of cellular activities of overexpressed full-length GEFs.
A new, single cell-based analysis was developed and used to enable the quantitative comparison of cellular activities of the overexpressed full-length GEFs.
Source:
Comparisons
Source-backed strengths
The assay was specifically developed for quantitative comparison of full-length GEF activities at the single-cell level. In primary human endothelial cells, it resolved differential Cdc42 activation efficiency, identifying PLEKHG2, FGD1, PLEKHG1, and PREX1 as the strongest activators among those tested, with FGD1 showing the highest selectivity.
Compared with free-energy calculations
single cell-based analysis and free-energy calculations address a similar problem space.
Shared frame: same top-level item type
Compared with mathematical model
single cell-based analysis and mathematical model address a similar problem space.
Shared frame: same top-level item type
Strengths here: looks easier to implement in practice.
Compared with SwiftLib
single cell-based analysis and SwiftLib address a similar problem space.
Shared frame: same top-level item type
Ranked Citations
- 1.