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MedChemExpress total rhoa
Total Rhoa, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/total+rhoa/RhoA+Antibody/pm41273843-104-31-32
Average 93 stars, based on 1 article reviews

total rhoa - by Bioz Stars, 2026-11

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Article Title: Fibrinogen drives neuroinflammation and neuropathology in perioperative neurocognitive disorders.
Article Snippet: Primary Antibodies: Phospho-P13K (Zenbio, 341468, 1:500), Total-P13K (Zenbio, Rabbit, 1:500), Phospho-Akt (Zenbio, 341790, 1:1000), Total Akt (Zenbio, 342529, 1:1000), CD11b (Servicebio, 20536–1-AP, 1:2000), Iba-1 (MCE, HY-P80501, 1:500), active-RhoA (UpingBio, YP-Ab-16,124, 1:1000), Total-RhoA (MCE, HYP80881, 1:1000), β-actin (Proteintech, A5441, 1:5000), PSD95 (Proteintech, 20665–1-AP, 1:20000), Synaptophysin (Proteintech, 17785–1- AP, 1:100000), Beta Tubulin (Proteintech, 80713–1-RR, 1:10000).

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A) Graphical overview of the applied commercially available dopaminergic (DA) differentiation kit for differentiating iPSC-derived PARK2 -/- NSCs and isogenic control NSCs. B-F) Immunofluorescence staining and quantification of β-tubulin-III + (BTUB, red), tyrosine hydroxylase (TH, green), microtubule-associated protein 2 (MAP2, red), synaptophysin (red), and glial-acidic fibrillary protein (GFAP, green) of differentiated cultures showed no difference in the differentiation capacity of PARK2 -/- and isogenic control cells or maturity of the neuronal cultures. Scale bar = 50 µm. Mean ± SEM, n = 6-9 coverslips per cell line from 2 independent differentiations. Statistical analysis: Student’s t-test. G) RhoA activity was significantly increased in PARK2 -/- neurons, measured from the ratio of GTP-bound RhoA to total RhoA levels. Mean ± SEM, n = 8 samples per cell line from 4 independent differentiations. Statistical analysis: Student’s t-test, ***p < 0.001. H) Graphical overview of the RhoA-inhibiting strategies applied in this study. RhoA activity was either inhibited by blocking GTP binding using rhosin (120 µM) or by preventing isoprenylation of RhoA by simvastatin (300 nM).

Journal: bioRxiv

Article Title: Simvastatin attenuates disease phenotypes in human induced pluripotent stem cell models of familial Parkinson’s disease through RhoA inhibition

doi: 10.64898/2026.08.26.747232

Figure Lengend Snippet: A) Graphical overview of the applied commercially available dopaminergic (DA) differentiation kit for differentiating iPSC-derived PARK2 -/- NSCs and isogenic control NSCs. B-F) Immunofluorescence staining and quantification of β-tubulin-III + (BTUB, red), tyrosine hydroxylase (TH, green), microtubule-associated protein 2 (MAP2, red), synaptophysin (red), and glial-acidic fibrillary protein (GFAP, green) of differentiated cultures showed no difference in the differentiation capacity of PARK2 -/- and isogenic control cells or maturity of the neuronal cultures. Scale bar = 50 µm. Mean ± SEM, n = 6-9 coverslips per cell line from 2 independent differentiations. Statistical analysis: Student’s t-test. G) RhoA activity was significantly increased in PARK2 -/- neurons, measured from the ratio of GTP-bound RhoA to total RhoA levels. Mean ± SEM, n = 8 samples per cell line from 4 independent differentiations. Statistical analysis: Student’s t-test, ***p < 0.001. H) Graphical overview of the RhoA-inhibiting strategies applied in this study. RhoA activity was either inhibited by blocking GTP binding using rhosin (120 µM) or by preventing isoprenylation of RhoA by simvastatin (300 nM).

Article Snippet: The ratio of active GTP-bound RhoA to total RhoA was measured using the G-LISA RhoA Activation Assay Biochem Kit (Cytoskeleton Inc.) and Total RhoA ELISA Kit (Cytoskeleton Inc.) according to the manufacturer’s protocol.

Techniques: Derivative Assay, Control, Immunofluorescence, Staining, Activity Assay, Blocking Assay, Binding Assay

A-B) Necrotic cell death was evaluated by LDH release and found increased in PARK2 -/- cultures compared to control cultures both at day 45 and 52. Direct RhoA inhibition decreased cell death in PARK2 -/- cultures. Mean ± SEM, n = 6-18 wells per group from 2-4 independent differentiations. C-D) Increased number of casp3 + -apoptotic cells in PARK2 -/- neuronal cultures at day 45 and 52. Treatment from day 18-45 and 38-52 decreased apoptotic cell death in the PARK2 -/- cultures. Mean ± SEM, n = 5-6 from 2 independent differentiations. E) Total cytokine release, as evaluated by the mean fold change in cytokines levels per cytokine investigated relative to control levels, was increased in PARK2 -/- cultures and decreased by treatment. F-G) Heatmap showing relative levels of the individual cytokines investigated (IL-8, IL-6, IFN-γ, IL-13, IL-12p70, TNF-α, IL-10, IL-1β, and IL-4) in F) PARK2 -/- cultures relative to control and in G) treated groups relative to vehicle group for each cell line. H) Specific concentrations detected for the individual cytokines, showing increased levels for all cytokines except IL-2 in PARK2 -/- cultures and treatment-induced decrease in the levels of most cytokines. Mean ± SEM, n = 8 samples per group from 3 independent differentiations. Statistical analysis: two-way ANOVA, *p < 0.05, **p < 0.01, ***p < 0.001.

Journal: bioRxiv

Article Title: Simvastatin attenuates disease phenotypes in human induced pluripotent stem cell models of familial Parkinson’s disease through RhoA inhibition

doi: 10.64898/2026.08.26.747232

Figure Lengend Snippet: A-B) Necrotic cell death was evaluated by LDH release and found increased in PARK2 -/- cultures compared to control cultures both at day 45 and 52. Direct RhoA inhibition decreased cell death in PARK2 -/- cultures. Mean ± SEM, n = 6-18 wells per group from 2-4 independent differentiations. C-D) Increased number of casp3 + -apoptotic cells in PARK2 -/- neuronal cultures at day 45 and 52. Treatment from day 18-45 and 38-52 decreased apoptotic cell death in the PARK2 -/- cultures. Mean ± SEM, n = 5-6 from 2 independent differentiations. E) Total cytokine release, as evaluated by the mean fold change in cytokines levels per cytokine investigated relative to control levels, was increased in PARK2 -/- cultures and decreased by treatment. F-G) Heatmap showing relative levels of the individual cytokines investigated (IL-8, IL-6, IFN-γ, IL-13, IL-12p70, TNF-α, IL-10, IL-1β, and IL-4) in F) PARK2 -/- cultures relative to control and in G) treated groups relative to vehicle group for each cell line. H) Specific concentrations detected for the individual cytokines, showing increased levels for all cytokines except IL-2 in PARK2 -/- cultures and treatment-induced decrease in the levels of most cytokines. Mean ± SEM, n = 8 samples per group from 3 independent differentiations. Statistical analysis: two-way ANOVA, *p < 0.05, **p < 0.01, ***p < 0.001.

Techniques: Control, Inhibition

A-B) Quantification of immunofluorescence staining for the outer mitochondrial membrane protein TOM20 (red) at day 35 of differentiation showed significantly increased TOM20 + -mitochondrial area per cell in PARK2 -/- cultures relative to isogenic control cultures, which were normalized by statin and rhosin treatment. Mean ± SEM, n = 9-15 coverslips per group from 3-5 independent differentiations. Statistical analysis: two-way ANOVA, *p < 0.05. C) Total cellular ATP levels were significantly decreased in PARK2 -/- neurons relative to control but were not improved by simvastatin or rhosin treatment. Mean ± SEM, n = 8 wells per group from 2 independent differentiations. Statistical analysis: two-way ANOVA, *p < 0.05. D-E) Immunofluorescence staining for the lysosomal marker LAMP1 (green) and quantification showed significantly increased LAMP1 + -lysosomal area in PARK2 -/- neurons relative to control. Mean ± SEM, n = 22 coverslips from 6 independent differentiations. Statistical analysis: Student’s t-test, *p < 0.05. F) Simvastatin and rhosin treatment significantly reduced the lysosomal area in PARK2 -/- neurons equal to the level in control neurons. Mean ± SEM, n = 15-22 coverslips per group from 6 independent differentiations. Statistical analysis: two-way ANOVA, *p < 0.05 ***p < 0.001. G) Activity of the lysosomal enzyme β-galactosidase was measured over time for control (blue) and PARK2 -/- (grey) with and without treatment. H) Calculation of specific β-galactosidase activity revealed increased activity upon direct RhoA inhibition and with a non-significant tendency for simvastatin. Mean ± SEM, n = 12 wells per group from 4 independent differentiations. Statistical analysis: one-way ANOVA, ***p < 0.001.

Journal: bioRxiv

Article Title: Simvastatin attenuates disease phenotypes in human induced pluripotent stem cell models of familial Parkinson’s disease through RhoA inhibition

doi: 10.64898/2026.08.26.747232

Figure Lengend Snippet: A-B) Quantification of immunofluorescence staining for the outer mitochondrial membrane protein TOM20 (red) at day 35 of differentiation showed significantly increased TOM20 + -mitochondrial area per cell in PARK2 -/- cultures relative to isogenic control cultures, which were normalized by statin and rhosin treatment. Mean ± SEM, n = 9-15 coverslips per group from 3-5 independent differentiations. Statistical analysis: two-way ANOVA, *p < 0.05. C) Total cellular ATP levels were significantly decreased in PARK2 -/- neurons relative to control but were not improved by simvastatin or rhosin treatment. Mean ± SEM, n = 8 wells per group from 2 independent differentiations. Statistical analysis: two-way ANOVA, *p < 0.05. D-E) Immunofluorescence staining for the lysosomal marker LAMP1 (green) and quantification showed significantly increased LAMP1 + -lysosomal area in PARK2 -/- neurons relative to control. Mean ± SEM, n = 22 coverslips from 6 independent differentiations. Statistical analysis: Student’s t-test, *p < 0.05. F) Simvastatin and rhosin treatment significantly reduced the lysosomal area in PARK2 -/- neurons equal to the level in control neurons. Mean ± SEM, n = 15-22 coverslips per group from 6 independent differentiations. Statistical analysis: two-way ANOVA, *p < 0.05 ***p < 0.001. G) Activity of the lysosomal enzyme β-galactosidase was measured over time for control (blue) and PARK2 -/- (grey) with and without treatment. H) Calculation of specific β-galactosidase activity revealed increased activity upon direct RhoA inhibition and with a non-significant tendency for simvastatin. Mean ± SEM, n = 12 wells per group from 4 independent differentiations. Statistical analysis: one-way ANOVA, ***p < 0.001.

Techniques: Immunofluorescence, Staining, Membrane, Control, Marker, Activity Assay, Inhibition

A-B) Western blotting for parkin showed significantly increased protein expression upon both simvastatin treatment and direct RhoA inhibition in control neurons and no parkin expression in PARK2 -/- neurons. C-D) Protein expression levels of NIX were increased in control cultures upon direct RhoA inhibition and showed a non-significant tendency for upregulation in the simvastatin-treated control group, as well as for treatment of PARK2 -/- neurons. E-G) Expression levels of LC3B quantified as both total LC3B levels (LC3B I + LC3B II) and LC3B turnover (LC3B II/ LC3B I) revealed significantly increased expression levels upon direct RhoA inhibition. H-I) P62 protein expression was elevated in PARK2 -/- neurons and reduced following simvastatin treatment. Protein expression levels were normalized to actin and are shown relative to the mean of all samples per differentiation. Mean ± SEM, n = 3-5 samples per group from 3-4 independent differentiations. Statistical analysis: two-way ANOVA, *p < 0.05, **p < 0.01, ***p < 0.001.

Journal: bioRxiv

Article Title: Simvastatin attenuates disease phenotypes in human induced pluripotent stem cell models of familial Parkinson’s disease through RhoA inhibition

doi: 10.64898/2026.08.26.747232

Figure Lengend Snippet: A-B) Western blotting for parkin showed significantly increased protein expression upon both simvastatin treatment and direct RhoA inhibition in control neurons and no parkin expression in PARK2 -/- neurons. C-D) Protein expression levels of NIX were increased in control cultures upon direct RhoA inhibition and showed a non-significant tendency for upregulation in the simvastatin-treated control group, as well as for treatment of PARK2 -/- neurons. E-G) Expression levels of LC3B quantified as both total LC3B levels (LC3B I + LC3B II) and LC3B turnover (LC3B II/ LC3B I) revealed significantly increased expression levels upon direct RhoA inhibition. H-I) P62 protein expression was elevated in PARK2 -/- neurons and reduced following simvastatin treatment. Protein expression levels were normalized to actin and are shown relative to the mean of all samples per differentiation. Mean ± SEM, n = 3-5 samples per group from 3-4 independent differentiations. Statistical analysis: two-way ANOVA, *p < 0.05, **p < 0.01, ***p < 0.001.

Techniques: Western Blot, Expressing, Inhibition, Control

A) 32 different PD patient and control iPSC-derived DA neuronal lines were screened for RhoA activity levels. B) Mean RhoA activity levels across the different PD-related gene mutations (PINK1 loss of function, parkin loss of function, LRRK2 (G2019S), LRRK2 (R1441C), GBA (L44P), GBA (N370S), SNCA (A53T), and SNCA (triplication)) show increased levels across all lines relative to control. Mean ± SEM, n = 3-5 cell lines per group. Statistical analysis: one-way ANOVA, *p < 0.05, ***p < 0.001.

Journal: bioRxiv

Article Title: Simvastatin attenuates disease phenotypes in human induced pluripotent stem cell models of familial Parkinson’s disease through RhoA inhibition

doi: 10.64898/2026.08.26.747232

Figure Lengend Snippet: A) 32 different PD patient and control iPSC-derived DA neuronal lines were screened for RhoA activity levels. B) Mean RhoA activity levels across the different PD-related gene mutations (PINK1 loss of function, parkin loss of function, LRRK2 (G2019S), LRRK2 (R1441C), GBA (L44P), GBA (N370S), SNCA (A53T), and SNCA (triplication)) show increased levels across all lines relative to control. Mean ± SEM, n = 3-5 cell lines per group. Statistical analysis: one-way ANOVA, *p < 0.05, ***p < 0.001.

Techniques: Control, Derivative Assay, Activity Assay

A. Diagram illustrating the effect of RhoA(Q63L) mutation on GTPase regulation. B. Schematic of lentiviruses construct encoding control (top) and RhoA(Q63L) mutant (bottom), all driven by the MND promoter. T2A and P2A encode two self-cleavage peptides. RQR8 is used for detection and purification of transduced cells. C. Representative flow cytometry data of purified RQR8+ T cells using PE -conjugated anti-CD34 (QBend10) antibody. D. Representative Western blots of whole cell lysate and RhoA-GTP pulldown samples with RBD beads with antibodies against RhoA and β-actin. Rho activating treatments were included to assess basal protein expression and activation levels in T cells. E. Representative immunofluorescence images of T cells stained with RhoA (red) and RhoA-GTP (green) antibodies, and counter stained with DAPI (blue). Scale bar: 50μm. F. Proliferation rate and viability of human T cells expressing control or RhoA(Q63L) over 7 days. G. Representative images of infiltrated T cell morphology in 3D collagen gels. Quantification of cell morphology parameters demonstrated reduced circularity and increased cell size in RhoA(Q63L) T cells compared to the control. Each dot represents an individual cell pooled from three independent experiments. Data are presented as mean ± s.e.m.

Journal: bioRxiv

Article Title: Engineering “physically optimized” T cells for increased sampling of complex tumor microenvironments

doi: 10.64898/2026.01.28.702394

Figure Lengend Snippet: A. Diagram illustrating the effect of RhoA(Q63L) mutation on GTPase regulation. B. Schematic of lentiviruses construct encoding control (top) and RhoA(Q63L) mutant (bottom), all driven by the MND promoter. T2A and P2A encode two self-cleavage peptides. RQR8 is used for detection and purification of transduced cells. C. Representative flow cytometry data of purified RQR8+ T cells using PE -conjugated anti-CD34 (QBend10) antibody. D. Representative Western blots of whole cell lysate and RhoA-GTP pulldown samples with RBD beads with antibodies against RhoA and β-actin. Rho activating treatments were included to assess basal protein expression and activation levels in T cells. E. Representative immunofluorescence images of T cells stained with RhoA (red) and RhoA-GTP (green) antibodies, and counter stained with DAPI (blue). Scale bar: 50μm. F. Proliferation rate and viability of human T cells expressing control or RhoA(Q63L) over 7 days. G. Representative images of infiltrated T cell morphology in 3D collagen gels. Quantification of cell morphology parameters demonstrated reduced circularity and increased cell size in RhoA(Q63L) T cells compared to the control. Each dot represents an individual cell pooled from three independent experiments. Data are presented as mean ± s.e.m.

Article Snippet: To examine total RhoA and RhoA-GTP, 1:50 rabbit anti-total RhoA (Novus Bio,Centennial, CO) and 1:100 mouse anti-RhoA-GTP (NewEast Biosciences, King of Prussia, PA) diluted in the blocking buffer were incubated with the T cells at 4°C overnight.

Techniques: Mutagenesis, Construct, Control, Purification, Flow Cytometry, Western Blot, Expressing, Activation Assay, Immunofluorescence, Staining

A. Fluorescence-lifetime images of control and RhoA(Q63L) T cells with Flipper-TR to assess cortical membrane tension. Cells are color-coded by fluorescence lifetime (red, shorter lifetimes; blue, longer lifetimes). B. Quantification of average fluorescence lifetimes across Z-stacks from Flipper-TR–stained T cells shows significantly longer lifetimes in RhoA(Q63L) cells, consistent with increased cortical contractility. C. Physics-based mathematical modeling predicts that increased cortical contractility results in increased T cell migration. D. Multiphoton time-lapse images of human control and RhoA(Q63L) T cells migrating in 3D collagen matrices. Representative single-cell migration tracks are highlighted in blue. Images were acquired every 1 min for 1 h. Colors: green, T cells; gray, collagen fibers. E. Motility coefficient for human control and RhoA(Q63L) T cells migrating in 3D collagen matrices. Each dot represents an individual tracked T cell. F. Average area sampled per frame by T cells migrating in 3D collagen matrices. n = 4 biological replicates. G. Multiphoton time-lapse images of murine control and RhoA(Q63L) and CD8⁺ T cells migrating within live KPCT pancreatic tumor slices. Colors: red, PDA carcinoma cells; green, T cells; gray, fibrillar collagen. H. Motility coefficients of murine control and RhoA(Q63L) CD8⁺ T cells migrating in tumor slices, showing a significant increase in motility in RhoA(Q63L) T cells. I. Representative multiphoton microscopy images showing the cumulative area sampled by infiltrating T cells in tumor slices over a 2-h period. Regions of high T-cell presence are outlined in green. J. Quantification of the percentage of area sampled per field of view per T cell. Data are presented as mean ± s.e.m. Statistical comparisons were performed using unpaired two-tailed t-tests with Welch’s correction.

Journal: bioRxiv

Article Title: Engineering “physically optimized” T cells for increased sampling of complex tumor microenvironments

doi: 10.64898/2026.01.28.702394

Figure Lengend Snippet: A. Fluorescence-lifetime images of control and RhoA(Q63L) T cells with Flipper-TR to assess cortical membrane tension. Cells are color-coded by fluorescence lifetime (red, shorter lifetimes; blue, longer lifetimes). B. Quantification of average fluorescence lifetimes across Z-stacks from Flipper-TR–stained T cells shows significantly longer lifetimes in RhoA(Q63L) cells, consistent with increased cortical contractility. C. Physics-based mathematical modeling predicts that increased cortical contractility results in increased T cell migration. D. Multiphoton time-lapse images of human control and RhoA(Q63L) T cells migrating in 3D collagen matrices. Representative single-cell migration tracks are highlighted in blue. Images were acquired every 1 min for 1 h. Colors: green, T cells; gray, collagen fibers. E. Motility coefficient for human control and RhoA(Q63L) T cells migrating in 3D collagen matrices. Each dot represents an individual tracked T cell. F. Average area sampled per frame by T cells migrating in 3D collagen matrices. n = 4 biological replicates. G. Multiphoton time-lapse images of murine control and RhoA(Q63L) and CD8⁺ T cells migrating within live KPCT pancreatic tumor slices. Colors: red, PDA carcinoma cells; green, T cells; gray, fibrillar collagen. H. Motility coefficients of murine control and RhoA(Q63L) CD8⁺ T cells migrating in tumor slices, showing a significant increase in motility in RhoA(Q63L) T cells. I. Representative multiphoton microscopy images showing the cumulative area sampled by infiltrating T cells in tumor slices over a 2-h period. Regions of high T-cell presence are outlined in green. J. Quantification of the percentage of area sampled per field of view per T cell. Data are presented as mean ± s.e.m. Statistical comparisons were performed using unpaired two-tailed t-tests with Welch’s correction.

Techniques: Fluorescence, Control, Membrane, Staining, Migration, Single Cell, Microscopy, Two Tailed Test

( A ) Representative multiphoton time-lapse images of murine RhoA(Q63L) and control CD8⁺ T cells migrating in 3D collagen matrices. Cell trajectories are overlaid and color-coded by total distance traveled (blue = short; red =long). Images were acquired every 1 min for 1 h. Colors: green, T cells; gray, collagen fibers. ( B ) Motility coefficient of murine RhoA(Q63L) and control CD8⁺ T cells migrating in 3D collagen matrices. Each dot represents an individual tracked T cell. ( C ) Total distance traveled by murine RhoA(Q63L) and control CD8⁺ T cells in 3D collagen matrices. Each dot represents an individual tracked T cell. ( D ) Average circularity of murine RhoA(Q63L) and control CD8⁺ T cells in 3D collagen matrices during the imaged period. A value of 1.0 indicates a perfect circle, and the value approaches 0 for elongated cells. ( E ) Cell size of murine RhoA(Q63L) and control CD8⁺ T cells in 3D collagen matrices measure using particle analyzer in FĲI. Data are presented as mean ± s.e.m.; statistical significance was determined using unpaired two-tailed t-tests with Welch’s correction.

Journal: bioRxiv

Article Title: Engineering “physically optimized” T cells for increased sampling of complex tumor microenvironments

doi: 10.64898/2026.01.28.702394

Figure Lengend Snippet: ( A ) Representative multiphoton time-lapse images of murine RhoA(Q63L) and control CD8⁺ T cells migrating in 3D collagen matrices. Cell trajectories are overlaid and color-coded by total distance traveled (blue = short; red =long). Images were acquired every 1 min for 1 h. Colors: green, T cells; gray, collagen fibers. ( B ) Motility coefficient of murine RhoA(Q63L) and control CD8⁺ T cells migrating in 3D collagen matrices. Each dot represents an individual tracked T cell. ( C ) Total distance traveled by murine RhoA(Q63L) and control CD8⁺ T cells in 3D collagen matrices. Each dot represents an individual tracked T cell. ( D ) Average circularity of murine RhoA(Q63L) and control CD8⁺ T cells in 3D collagen matrices during the imaged period. A value of 1.0 indicates a perfect circle, and the value approaches 0 for elongated cells. ( E ) Cell size of murine RhoA(Q63L) and control CD8⁺ T cells in 3D collagen matrices measure using particle analyzer in FĲI. Data are presented as mean ± s.e.m.; statistical significance was determined using unpaired two-tailed t-tests with Welch’s correction.

Techniques: Control, Two Tailed Test

A. Fluorescence lifetime imaging of control and RhoA(Q63L) T cells inside 3D collagen matrices. Left: unstimulated; right: stimulated with anti-CD3/CD28 antibodies; Color bar indicates percentage of NAD(P)H α1from FLIM analysis (red: low percentage; blue: high percentage). B. Quantification of NAD(P)H α1 percentage in unstimulated and CD3/CD28-stimulated control and RhoA(Q63L) T cells. RhoA(Q63L) T cells showed significantly elevated baseline α1 levels, indicating increased activation. C-D. Multiparameter flow cytometry analysis of T cell subpopulations. RhoA(Q63L) modified T cells display a higher frequency of CD8⁺ T cells (C) and effector subsets (D) compared to control T cells. E. Heatmap of T cell percentage across differentiation stages: naïve (Tn), central memory (Tcm), effector memory (Tem), and terminally differentiated effector (E) cells, showing as heatmap. RhoA(Q63L) modified T cells exhibited a more differentiated phenotype, with the majority residing in the Tem3 (∼60%) and E (∼15%) subsets. F. Expression of exhaustion markers PD-1 and LAG-3 on T cells. RhoA(Q63L) modified T cells exhibit reduced PD-1 and LAG-3 expression compared to control T cells, suggesting a less exhausted phenotype.

Journal: bioRxiv

Article Title: Engineering “physically optimized” T cells for increased sampling of complex tumor microenvironments

doi: 10.64898/2026.01.28.702394

Figure Lengend Snippet: A. Fluorescence lifetime imaging of control and RhoA(Q63L) T cells inside 3D collagen matrices. Left: unstimulated; right: stimulated with anti-CD3/CD28 antibodies; Color bar indicates percentage of NAD(P)H α1from FLIM analysis (red: low percentage; blue: high percentage). B. Quantification of NAD(P)H α1 percentage in unstimulated and CD3/CD28-stimulated control and RhoA(Q63L) T cells. RhoA(Q63L) T cells showed significantly elevated baseline α1 levels, indicating increased activation. C-D. Multiparameter flow cytometry analysis of T cell subpopulations. RhoA(Q63L) modified T cells display a higher frequency of CD8⁺ T cells (C) and effector subsets (D) compared to control T cells. E. Heatmap of T cell percentage across differentiation stages: naïve (Tn), central memory (Tcm), effector memory (Tem), and terminally differentiated effector (E) cells, showing as heatmap. RhoA(Q63L) modified T cells exhibited a more differentiated phenotype, with the majority residing in the Tem3 (∼60%) and E (∼15%) subsets. F. Expression of exhaustion markers PD-1 and LAG-3 on T cells. RhoA(Q63L) modified T cells exhibit reduced PD-1 and LAG-3 expression compared to control T cells, suggesting a less exhausted phenotype.

Techniques: Fluorescence, Imaging, Control, Activation Assay, Flow Cytometry, Modification, Expressing

( A ) Schematic representation of vector constructs encoding mesothelin-targeted CAR (mesoCAR) T cells with or without the RhoA(Q63L) mutation. ( B )Representative flow cytometry data of purified mesoCAR RQR8+ T cells using PE -conjugated anti-CD34 (QBend10) antibody. ( C ) Western blots of whole cell lysate and RhoA-GTP pulldown samples with RBD beads with antibodies of RhoA and β-actin.

Journal: bioRxiv

Article Title: Engineering “physically optimized” T cells for increased sampling of complex tumor microenvironments

doi: 10.64898/2026.01.28.702394

Figure Lengend Snippet: ( A ) Schematic representation of vector constructs encoding mesothelin-targeted CAR (mesoCAR) T cells with or without the RhoA(Q63L) mutation. ( B )Representative flow cytometry data of purified mesoCAR RQR8+ T cells using PE -conjugated anti-CD34 (QBend10) antibody. ( C ) Western blots of whole cell lysate and RhoA-GTP pulldown samples with RBD beads with antibodies of RhoA and β-actin.

Techniques: Plasmid Preparation, Construct, Mutagenesis, Flow Cytometry, Purification, Western Blot

A. Migration of RhoA(Q63L) modified and control mesoCAR T cells in 3D collagen matrices. Migration trajectories are overlaid on time-lapse images and color-coded by total distance traveled (blue, short; red, long). RhoA(Q63L) modified CAR T cells display increased motility and more persistent movement. B. Quantification of mesoCAR T-cell motility coefficients in 3D collagen matrices. RhoA(Q63L) modified CAR T cells exhibit significantly higher motility coefficients than control CAR T cells. C. Quantification of 2D cytotoxicity. mesoCAR and mesoCAR RhoA(Q63L) modified T cells. Both CAR T-cell groups show similar increases in target-cell killing with increasing effector ratios. D. Multiphoton images of mesoCAR and mesoCAR RhoA(Q63L) modified T cells migrating and interacting with AsPC-1 cells in 3D collagen matrices. Colors: green, T cells; red, AsPC-1 cells; gray, collagen fibers. E. Quantification of T-cell–AsPC-1 interaction events per T cell for mesoCAR, and mesoCAR RhoA(Q63L) modified T-cell groups in 3D collagen matrices. F. Quantification of T-cell–AsPC-1 interactions events per carcinoma cell for mesoCAR and mesoCAR RhoA(Q63L) modified T-cell groups in 3D collagen matrices. G. Quantification of mesoCAR and mesoCAR RhoA(Q63L) modified T-cell motility in collagen matrices containing AsPC-1 cells. H. Quantification of mesoCAR and mesoCAR RhoA(Q63L) modified T-cell motility in collagen regions lacking AsPC-1 cells. I. Multiphoton microscopy images showing the cumulative area explored by mesoCAR, and mesoCAR RhoA(Q63L) modified T cells in AsPC-1–embedded 3D collagen matrices. Overlaid tracks and projected cumulative areas over 90 min are shown (red, AsPC-1 cells; yellow, T-cell area coverage). Data are presented as mean ± s.e.m. Statistical comparisons were performed using unpaired two-tailed t-tests with Welch’s correction.

Journal: bioRxiv

Article Title: Engineering “physically optimized” T cells for increased sampling of complex tumor microenvironments

doi: 10.64898/2026.01.28.702394

Figure Lengend Snippet: A. Migration of RhoA(Q63L) modified and control mesoCAR T cells in 3D collagen matrices. Migration trajectories are overlaid on time-lapse images and color-coded by total distance traveled (blue, short; red, long). RhoA(Q63L) modified CAR T cells display increased motility and more persistent movement. B. Quantification of mesoCAR T-cell motility coefficients in 3D collagen matrices. RhoA(Q63L) modified CAR T cells exhibit significantly higher motility coefficients than control CAR T cells. C. Quantification of 2D cytotoxicity. mesoCAR and mesoCAR RhoA(Q63L) modified T cells. Both CAR T-cell groups show similar increases in target-cell killing with increasing effector ratios. D. Multiphoton images of mesoCAR and mesoCAR RhoA(Q63L) modified T cells migrating and interacting with AsPC-1 cells in 3D collagen matrices. Colors: green, T cells; red, AsPC-1 cells; gray, collagen fibers. E. Quantification of T-cell–AsPC-1 interaction events per T cell for mesoCAR, and mesoCAR RhoA(Q63L) modified T-cell groups in 3D collagen matrices. F. Quantification of T-cell–AsPC-1 interactions events per carcinoma cell for mesoCAR and mesoCAR RhoA(Q63L) modified T-cell groups in 3D collagen matrices. G. Quantification of mesoCAR and mesoCAR RhoA(Q63L) modified T-cell motility in collagen matrices containing AsPC-1 cells. H. Quantification of mesoCAR and mesoCAR RhoA(Q63L) modified T-cell motility in collagen regions lacking AsPC-1 cells. I. Multiphoton microscopy images showing the cumulative area explored by mesoCAR, and mesoCAR RhoA(Q63L) modified T cells in AsPC-1–embedded 3D collagen matrices. Overlaid tracks and projected cumulative areas over 90 min are shown (red, AsPC-1 cells; yellow, T-cell area coverage). Data are presented as mean ± s.e.m. Statistical comparisons were performed using unpaired two-tailed t-tests with Welch’s correction.

Techniques: Migration, Modification, Control, Microscopy, Two Tailed Test

( A ) The mesoCAR RhoA(Q63L) cells showed increased displacement, ( B ) mean speed, and ( C ) less confined movement.

Journal: bioRxiv

Article Title: Engineering “physically optimized” T cells for increased sampling of complex tumor microenvironments

doi: 10.64898/2026.01.28.702394

Figure Lengend Snippet: ( A ) The mesoCAR RhoA(Q63L) cells showed increased displacement, ( B ) mean speed, and ( C ) less confined movement.

Techniques:

MesoCAR and mesoCAR RhoA(Q63L) T cells were co-cultured with AsPC-1 at varying effector-to-target ratios. The percentage of viable AsPC-1 cells is shown relative to no-T-cell controls.

Journal: bioRxiv

Article Title: Engineering “physically optimized” T cells for increased sampling of complex tumor microenvironments

doi: 10.64898/2026.01.28.702394

Figure Lengend Snippet: MesoCAR and mesoCAR RhoA(Q63L) T cells were co-cultured with AsPC-1 at varying effector-to-target ratios. The percentage of viable AsPC-1 cells is shown relative to no-T-cell controls.

Techniques: Cell Culture

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