EMBO/soda-nel huggingface dataset:
TRIM50 promotes NLRP3 inflammasome activation by directly inducing NLRP3 oligomerization (2022)
Figure 4

Figure 4. TRIM50 promotes NLRP3 inflammasome activation by inducing NLRP3 oligomerization.

A. SDD-AGE analysis of NLRP3 oligomerization in HEK293T cells transfected with NLRP3 and TRIM50 plasmids.

B. SDD-AGE analysis of NLRP3 oligomerization in NLRP3 and TRIM50 transfected HEK293T cells followed with nigericin treatment for 30min.

C. Immunoblot analysis of ASC oligomerization in cross-linked cytosolic pellets (insoluble) and whole cell lysate (soluble) in HEK293T cells transfected with NLRP3, ASC and TRIM50 plasmids followed with nigericin treatment for 30 min.

D. SDD-AGE analysis of NLRP3 oligomerization in WT or Trim50-/- peritoneal macrophages with LPS treatment for 6h and ATP treatment for 30 min.

E. Immunoblot analysis of ASC oligomerization in cross-linked cytosolic pellets (insoluble) and whole cell lysate (soluble) in WT or Trim50-/- peritoneal macrophages by LPS stimulation for 6h and ATP treatment for 30min.

F. SDD-AGE analysis of NLRP3 oligomerization in WT or Trim50-/- BMDM cells with LPS treatment for 6h and ATP treatment for 30 min.

G. Immunoblot analysis of ASC oligomerization in cross-linked cytosolic pellets (insoluble) and whole cell lysate (soluble) in WT or Trim50-/- BMDM cells by LPS stimulation for 6h and ATP treatment for 30min.

H. SDD-AGE analysis of the oligomerization of NLRP3 in HEK293T cells transfected with His-NLRP3 and TRIM50 or TRIM50(ΔRING) mutant.

I. In vitro NLRP3 oligomerization assay with in-vitro translated TRIM50 and NLRP3 proteins.

J. Immunoprecipitation analysis of NLRP3 ubiquitination in HA-ubiquitin, His-NLRP3 and Myc-TRIM50 transfected HEK293T cells with further treatment with tranilast or MCC950 for 24h.

Data information: Data are representative of three biological replicates with similar results.
TRIM50 promotes NLRP3 inflammasome activation by directly inducing NLRP3 oligomerization (2022)
Figure 5

Figure 5. The coiled-coil domains of TRIM50 are required for the regulation of the NLRP3 inflammasome.

A. Immunoprecipitation analysis of NLRP3 ubiquitination in HEK293T cells transfected with NLRP3, HA-Ubiquitin, TRIM50 or its truncation mutants.

B. SDD-AGE analysis of NLRP3 oligomerization in NLRP3 together with TRIM50 or its coiled-coil domain-deleted mutants (ΔC-C1 and ΔC-C2) transfected HEK293T cells.

C. SDD-AGE analysis of the oligomerization of TRIM50 in TRIM50 or its coiled-coil domain-deleted mutants (ΔC-C1 and ΔC-C2) transfected HEK293T cells.

D. SDD-AGE analysis of the oligomerization of NLRP3 and TRIM50 in HEK293T cells overexpressing NLRP3 together with TRIM50 or its coiled-coil domain-deleted mutants.

E. Immunoblot analysis of NLRP3 in HEK293T cells transfected with NLRP3 plasmid and TRIM50 coiled-coil domain-deleted mutants, followed with the cycloheximide (CHX) treatment for 0h, 4h or 8h.

F. Immunoblot analysis of ASC oligomerization in cross-linked cytosolic pellets (insoluble) and whole cell lysate(soluble) in HEK293T cells transfected with His-NLRP3 and TRIM50 or TRIM50 coiled-coil domain-deleted mutants.

Data information: Band densities were quantitated by 'Image J' software and normalized to GAPDH. P-values are shown, two-way ANOVA(E). Data are representative of three biological replicates with similar results. (mean ± SD in E).
TRIM50 promotes NLRP3 inflammasome activation by directly inducing NLRP3 oligomerization (2022)
Figure 6

Figure 6. TRIM50 regulates NLRP3 inflammasome-related diseases in mice.

A. Survival status of WT and Trim50-/- mice after intraperitoneal injection with LPS (n=10 mice/group).

B. ELISA analysis of IL-1β, TNF-α and IL-6 in serum of WT or Trim50-/- mice after i.p. injection with LPS for 6h (n=4-6 mice/group).

C. Histopathological analysis of the lung tissues by hematoxylin and eosin (H&E) staining. The quantified lung injury was depicted by defined clinical parameters in ALI score (n=6 mice/group). Scale bars: 50μm.

D. Flow cytometry analysis of the neutrophils (left) and Ly6C+ monocytes (right) in peritoneum of WT or Trim50-/- mice after i.p. injection with Alum. (n=6 mice/group).

E. WT or Trim50-/- mice were i.p. injected with FA for 36h, followed with immunoblot analysis of NLRP3, pro-IL-1β, Caspase1 p20, IL-1β in the kidney tissue samples.

F. H&E staining of kidney tissue sections. Scale bars: 20μm.

G. Periodic-acid-Schiff (PAS) staining of kidney tissue sections. Scale bars: 20μm.

H. Schematic diagram of the regulatory role of TRIM50 in NLRP3 inflammasome activation.

Data information: P-values are shown, two-way ANOVA (A) or two-tailed Student's t-test (B-E). Data are representative of three biological replicates with similar results. (mean ± SD in A-E).

Expanded View Figure legends
Epstein-Barr virus derived circular RNA LMP2A induces stemness in EBV-associated gastric cancer (2020)
Figure 1

Fig. 1. EBVaGC CSCs are selectively enriched under low dose chemotherapy pressure.

(A) Schematic model presenting the process used to acquire EBVaGC CSCs.

(B) Tumour growth curves for successive four-generation xenografts treated with 5-Fu or PBS. Twelve mice per group.

(C) Representative cases show the first and fourth generation xenograft H&E staining (left) and EBER-1 ISH staining (right).

(D) The morphology of parental SNU719 and SNU-4th cells.

(E) Tumour sphere culture was performed to evaluate the sphere formation capacity in SNU719 and SNU-4th cells, and the data are shown as the mean numbers and sizes of the tumour spheres. The central horizontal lines represent the median, the top and the bottom positions of the box represent upper and lower quartiles, error bars represent the mean ± SD, and the average number and maximal diameter of spheres were calculated under a microscope in five randomly chosen fields in each independent experiment, n=3 biological replicates.

(F) CCK8 assay of SNU719 and SNU-4th cells to determine cell proliferation under the indicated culture conditions (10% FBS or 0.1% FBS).

(G-H) Expression of stemness markers (Sox2, Klf4, Bmi1, Oct4) and drug resistance genes (ABCG2, Mrp1) evaluated by real-time PCR (G) and WB (H) in SNU719 and SNU-4th cells.

(I) Real-time PCR analysis of the expression of EMT-associated markers (E-cad, vimentin) and transcription factors (Twist1, Snail, Slug, Zeb1) in SNU719 and SNU-4th cells.

(J) WB analysis of the expression of E-cad, vimentin and Mmp7 in SNU719 and SNU-4th cells.

(K) Colony formation assay analysis of the colony-forming ability in SNU719 and SNU-4th cells.

(L) Transwell migration and the Matrigel invasion assay were performed to assess the migratory and invasive capability of SNU719 and SNU-4th cells.

(M) Representative images of the flow cytometric analysis of SP cells.

(N) Representative images of the flow cytometric analysis of the surface antigen phenotype.

Data information: Results are presented as the mean ± SD, n=3 biological replicates, scale bars =100 µm, *P < 0.05; **P < 0.01; *** P < 0.001, Student's t-test.
Epstein-Barr virus derived circular RNA LMP2A induces stemness in EBV-associated gastric cancer (2020)
Figure 3

Fig. 3. Characterization of circLMP2A in SNU-4th, SNU719 and YCCEL1 cells and correlated with the prognosis of EBVaGC patients.

(A) Schematic illustration showing the genomic loci of the circLMP2A (black arrow). The sequence of circLMP2A was validated by Sanger sequencing. The red arrow indicates the "head-to-tail" splicing sites of circLMP2A.

(B) Real-time PCR analysis of the expression of circLMP2A in SNU-4th, SNU719 and YCCEL1 cells.

(C) The existence of circLMP2A was validated by RT-PCR (up) and real-time PCR (down) in SNU-4th, SNU719 and YCCEL1 cells treated with or without RNase R digestion. GAPDH was used as a negative control.

(D) Real-time PCR analysis of circLMP2A and LMP2A expression after treatment with actinomycin D at the indicated time points in SNU-4th cells.

(E) Real-time PCR analysis of circLMP2A and LMP2A expression in either the cytoplasm or nucleus in SNU-4th cells. GAPDH and U6 were used as controls in cytoplasm and nucleus, respectively.

(F) RNA ISH for circLMP2A. U6 and 18S are mainly localized in the nucleus and cytoplasm, respectively, and were used as controls.

(G) Kaplan-Meier survival curve analysis showing the correlation between circLMP2A expression and OS. n= 69, P < 0.001, log-rank test.

(H) Kaplan-Meier survival curve analysis showing the correlation between circLMP2A expression and progression-free survival (PFS). n = 69, P < 0.001, log-rank test.

Data information: Results are presented as the mean ± SD, n=3 biological replicates, scale bar =10µm, *** P < 0.001, Student's t-test.
Epstein-Barr virus derived circular RNA LMP2A induces stemness in EBV-associated gastric cancer (2020)
Figure 4

Fig. 4. Silencing of circLMP2A inhibits the stemness phenotypes of SNU-4th cells.

(A) Real-time PCR analysis of the interfering efficacy and linear LMP2A mRNA levels after transfection of three circLMP2A shRNAs.

(B) Tumour sphere culture analysis of the tumour sphere formation in SNU-4th cells transfected with sh-circLMP2A-2, sh-circLMP2A-3 or sh-control. The central horizontal lines represent the median, top and bottom positions of the box represent upper and lower quartiles, and error bars represent the mean ± SD. The average number and maximal diameter of spheres were calculated under a microscope in five randomly chosen fields in each independent experiment, n=3 biological replicates. Scale bars =100µm.

(C-D) EMT-related markers, stemness markers and drug resistance genes were evaluated by real-time PCR (C) and WB (D) in SNU-4th cells transfected with sh-circLMP2A-2, sh-circLMP2A-3 or sh-control.

(E-F) Transwell assay (E) and colony formation assay (F) analysis of the migratory and invasive capability and colony-forming ability in SNU-4th cells transfected with sh-circLMP2A-2, sh-circLMP2A-3 or sh-control. Scale bars =100µm.

(G-H) Flow cytometric analysis of the rate of SP cells (G) and apoptosis (H) in SNU-4th cells transfected with sh-circLMP2A-2, sh-circLMP2A-3 or sh-control.

(I-J) Subcutaneously established tumour xenografts in NOD/SCID mice. Tumour volume (I) and tumour weight (J) of the xenografts were remarkably inhibited by down-regulation of circLMP2A. Six mice per group.

(K-L) Representative images of bioluminescence (K) and lung metastases (L) are presented to measure the metastatic colonies. Six mice per group, scale bars =50µm.

Data information: Results are presented as the mean ± SD, n=3 biological replicates, *P < 0.05; **P < 0.01; *** P < 0.001, Student's t-test).
Epstein-Barr virus derived circular RNA LMP2A induces stemness in EBV-associated gastric cancer (2020)
Figure 6

Fig. 6. circLMP2A serves as a sponge for miR-3908.

（A）Schematic illustration showing overlapping target miRNAs of circLMP2A predicted by miRanda and TargetScan.

(B) The relative levels of 7 miRNA candidates were detected by real-time PCR in SNU719 and SNU-4th cells.

(C-E) Real-time PCR analysis of 7 miRNA expression in SNU-4th cells transfected with sh-circLMP2A-2 or sh-control (C), and SNU719 (D) and YCCEL1 cells (E) transfected with circLMP2A or vector.

(F-H) circLMP2A in SNU-4th cell lysate was pulled down with circLMP2A specific probe and detected by real-time PCR (F) and RT-PCR (H). The relative levels of 5 miRNA candidates were detected by real-time PCR (G) and RT-PCR (H). GAPDH was used as a negative control.

(I) RNA ISH showing the co-localization between circLMP2A and miR-3908 in SNU-4th cells. circLMP2A probes were labelled with Cy3, and miR-3908 probes were labelled with FITC. Nuclei were stained with DAPI.

(J) Wild type and mutant circLMP2A and miR-3908 sequences are presented. Red font indicates mutant bases.

(K) Dual luciferase reporter assay for luciferase activity of the indicated plasmids (circLMP2A Wt, circLMP2A mut1, circLMP2A mut2, circLMP2A mut3 luciferase reporter) in HEK-293T cells transfected with mimic-NC or miR-3908.

Data information: Results are presented as the mean ± SD, n=3 biological replicates, scale bar =5µm, *P < 0.05; **P < 0.01; *** P < 0.001, Student's t-test.
Epstein-Barr virus derived circular RNA LMP2A induces stemness in EBV-associated gastric cancer (2020)
Figure 7

Fig. 7. Over-expression of miR-3908 reverses the circLMP2A induced stemness phenotype.

(A) Tumour sphere culture analysis of the tumour sphere formation ability of SNU-4th cells transfected with the above different mimics.

(B-C) Real-time PCR (B) and WB (C) analysis of EMT-related markers, stemness markers and drug resistance genes expression in SNU-4th cells transfected with the above different mimics.

(D-E) Colony formation assay (D) and transwell assay (E) analysis of the colony-forming ability and migratory and invasive capability of SNU-4th cells transfected with the above different mimics.

(F-G) Flow cytometric analysis of the rate of apoptosis (F) and SP cells (G) in SNU-4th cells transfected with the above different mimics.

(H) Pearson correlation analysis of the correlation between the expression of circLMP2A and miR-3908. n = 69, P = 0.039, Pearson's correlation coefficient analysis.

(I) Kaplan-Meier survival curves analysis of the correlation between miR-3908 expression and OS. n = 69, P = 0.049, log-rank test.

Data information: Results are presented as the mean ± SD, n=3 biological replicates, scale bars =100µm, *P < 0.05; **P < 0.01; *** P < 0.001, Student's t-test.
Epstein-Barr virus derived circular RNA LMP2A induces stemness in EBV-associated gastric cancer (2020)
Figure 8

Fig. 8. circLMP2A modulates the expression of miR-3908 target TRIM59.

(A) Schematic representation of the putative binding sites for miR-3908 and TRIM59.

(B) Dual luciferase reporter assay for the luciferase activity of the indicated plasmids (TRIM59-Wt and TRIM59-Mut luciferase reporter) in HEK-293T cells transfected with mimic-NC or miR-3908.

(C) Real-time PCR analysis of the mRNA level of TRIM59 in SNU719 and SNU-4th cells.

(D-F) Real-time PCR analysis of the expression of TRIM59 in SNU-4th (D), SNU719 (E) and YCCEL1 cells (F) transfected with the above different mimics.

(G-I) WB analysis of the expression of TRIM59 and p53 in SNU-4th (G), SNU719 (H) and YCCEL1 cells (I) transfected with the above different mimics.

(J) Immunohistochemical staining showing that over-expression of circLMP2A could lead to increased expression of TRIM59 and ERG but decreased expression of p53.

(K) WB analysis of the expression of TRIM59 and p53 in tumour xenografts.

(L)Immunohistochemical staining showing that high expression of circLMP2A in EBVaGC tissues resulted in significant increases in CD44+ CD24- cells and significant decreases in p53+ cells.

Data information: Results are presented as the mean ± SD, n=3 biological replicates, scale bars = 50µm, *P < 0.05; **P < 0.01; *** P < 0.001, Student's t-test.

Expanded View Figure legends
Cell death control: the interplay of apoptosis and autophagy in the pathogenicity of Sclerotinia sclerotiorum. (2013)
Figure 1

Expression of <italic>ced-9</italic> in <italic>Arabidopsis</italic> inhibits wild type infection but does not affect the A2 phenotype.

Agar plugs containing actively growing cultures of wild type S. sclerotiorum (strain 1980) and the OA deficient A2 mutant were inoculated onto Col-0 and ced-9 expressing Arabidopsis leaves. (A) Wild type inoculations onto Col-0 plants resulted in typical lesions for this pathogen including a rapid, spreading cell death; however, infection was completely suppressed in ced-9 expressing plants. The expression of this gene had no effect on the A2 phenotype. (B) Trypan blue staining indicates the extent of cell death for each genotype/strain combination, including an agar plug control. All images were recorded 48 hours post inoculation.
Cell death control: the interplay of apoptosis and autophagy in the pathogenicity of Sclerotinia sclerotiorum. (2013)
Figure 6

Oxidant accumulation in wild type and <italic>atg</italic> mutant plants.

(A) NBT treated Arabidopsis (Col-0 and two independent atg8a mutant lines) following agar plug inoculation with the A2 mutant. Images were collected 48 hours post inoculation. Dotted lines represent the edge of the observable legion. (B) RT-PCR was used to evaluate the transcript levels of three catalases (CAT1, 2, and 3) and three superoxide dismutases in Col-0 plants following inoculation with wild type S. sclerotiorum (black bars) and the A2 mutant strain (grey bars). *>2 fold change, **>5 fold change.
Lam6 Regulates the Extent of Contacts between Organelles. (2015)
Figure 2

Lam6 Is Localized to Several Cellular Contact Sites

(A) Fluorescence microscopy demonstrates that Lam6-GFP co-localizes with ERMES (Mdm34-Cherry) (yellow arrows) and also localizes to non-ERMES locations in the cell (red arrows). These additional locations co-localized with the NVJ (Nvj1-GFP) as well as with the vCLAMP (GFP-Vps39). Scale bar represents 5 μm.

(B) Overexpression and tagging of Lam6 confirmed that it co-localizes with ERMES (Mdm34-GFP) (yellow arrows) as well as to additional contact sites (red arrows), NVJ (marked by Nvj1) and vCLAMP (marked by Vps39). Scale bar represents 5 μm.
Lam6 Regulates the Extent of Contacts between Organelles. (2015)
Figure 3

Overexpression and Tagging of Lam6 Affects the Extent of Contact Sites

(A) Fluorescence microscopy demonstrates that the overexpression of Cherry-Lam6 (OE-Cherry-LAM6) results in an expansion of the following three contact sites: ERMES (Mdm34-GFP), NVJ (Nvj1-GFP), and vCLAMP (GFP-Vps39). This suggests that an increase in Lam6 levels in the contact site is sufficient for its expansion. The numbers represent the average contact site size (120 cells per sample). Scale bar represents 5 μm.

(B) Immuno-EM verified that GFP-Lam6 overexpression indeed causes an expansion of contact site size. While vCLAMP was hardly visible in WT cells, it could be detected easily in the OE strain (albeit often had ER tubules invading it). The NVJ underwent expansion as well as evoked PMN in OE strains, and the ER-mitochondria contact became large and elongated instead of small and distinct. N, nucleus; M, mitochondria; V, vacuole. Scale bar represents 200 nm (see also Figure S3I).
Lam6 Regulates the Extent of Contacts between Organelles. (2015)
Figure 4

Lam6 Is Important for Cross-Talk between Contact Sites

(A) Fluorescent microscopy shows that the ERMES contact (as measured by the number of Mdm34-GFP puncta per cell) expanded in the Δvps39 background relative to WT. However, the expansion did not occur on the background of Δvps39 Δlam6, demonstrating that Lam6 is necessary for ERMES expansion under these conditions. Scale bar represents 5 μm.

(B) Quantitation of (A). Bars represent the percentage of cells containing the specific number of puncta/cell out of total cells counted for the strain (for WT, n = 234 cells; for Δvps39, n = 246; for Δvps39 Δlam6, n = 271).

(C) Fluorescent microscopy demonstrates that downregulating ERMES contacts (by growing GALp-MDM34 strains in glucose) indeed caused expansion of vCLAMP (GFP-Vps39). However, this expansion was diminished in a Δlam6 background. Scale bar represents 5 μm (see also Figure S4).

(D) A model summarizing our hypothesis on the way that Lam6 functions to regulate contact site communication. In normal cells, where all contact sites are intact, Lam6 is found mostly in ERMES contact sites, and to a lesser extent in vCLAMP and NVJ. However, in case a contact site is lost, the Lam6 proteins that were localized to this contact become free to associate with the other contact sites, thus signaling that they must expand. Raising Lam6 levels in any other way in a contact site therefore would cause an expansion of this contact site.
Nox4 regulates InsP3 receptor-dependent Ca2+ release into mitochondria to promote cell survival (2020)
Figure 1

Figure 1. Nox4 inhibits mPT-dependent regulated cell death.

A, B Quantification of Nox4 mRNA levels (A) and protein levels (B) in cultured rat cardiomyocytes after increasing degrees of serum starvation as compared to serum-replete cells (15% serum). n=4 cell preparations/group. A representative immunoblot for Nox4 and tubulin as a loading control is shown in panel B.

C Cell death after 48 h serum starvation in cardiomyocytes in which Nox4 was depleted by an adenoviral shRNA (Ad.shNox4) as compared to cells infected with a control vector (Ad.Ctl). n=6/group. The representative immunoblot shows reduction in Nox4 protein levels after shRNA-mediated knockdown.

D Lactate dehydrogenase (LDH) activity in cell supernatants. Staurosporine (Stauro, 1 μmol/L) was used to induce cell death by apoptosis. n=4 cell preparations/group.

E Levels of high mobility group box1 protein (HMGB1) in cell supernatants. n=3/group. A representative immunoblot is shown at the top.

F Protein levels of cytochrome c in the cytoplasmic fractions of cardiomyocytes. n=4/group. A representative immunoblot is shown at the top. The cellular membrane fraction (Mem) containing mitochondria was used as a positive control.

G Percentage of Nox4-depleted and control cells with depolarized mitochondria, quantified by flow cytometry. n=3 cell preparations/group (100,000 cells per experiment).

H Effect of cyclosporin A (CsA, 1 μmol/L) on the percentage of cells with depolarized mitochondria. n=6-8/group.

I Effect of cyclosporin A (CsA, 1 μmol/L) on cell death in serum-starved cardiomyocytes. n=4/group.

J Cell death in serum starved Nox4 knockout MEFs (Nox4KO) and wild-type MEFs (WT). Cat = PEG-catalase (500 U/mL). Nox4KO MEFs were transfected either with active Nox4 or a catalytic inactive Nox4 mutant, Nox4P437H (Mut). n=6-12/group.

K HMGB1 levels in the supernatants of serum-starved MEFs in similar experiments to those in (J). n=4/group. A representative immunoblot is shown to the top.

L Percentage of MEFs with depolarized mitochondria. n=6/group.

Data information: Data are mean ± SEM. * P<0.05; ** P<0.01; *** P<0.001; **** P<0.0001 among compared groups or vs control. # P<0.05; #### P<0.0001 vs Nox4KO. C and G, 2-way ANOVA; all other panels, 1-way ANOVA.
Nox4 regulates InsP3 receptor-dependent Ca2+ release into mitochondria to promote cell survival (2020)
Figure 2

Figure 2. Nox4 regulates calcium transfer to mitochondria.

A Basal mitochondrial calcium levels assessed in serum-starved rat cardiomyocytes using a mitochondrial-targeted cameleon CFP/YFP FRET probe. Nox4 was depleted with silencing RNAs (siRNAs) or cells were transfected with a control scrambled siRNA (siScr). Representative photomicrographs are shown at the top. The spectrum color scale represents the ratio of emitted fluorescence (YFP/CFP). The mean changes in Nox4-depleted cells as compared to scrambled control (dotted line) at the bottom. The representative immunoblot shows depletion of Nox4 protein levels. Scale bars: 10 µm. n=3/group (with >50 cells per individual experiment).

B Basal mitochondrial calcium levels in WT and Nox4KO MEFs after serum starvation. Representative photomicrographs are shown at the top. The spectrum color scale represents the ratio of emitted fluorescence (YFP/CFP). Mean data at the bottom. Scale bars: 10 µm. n=3/group (with >100 cells per individual experiment).

C, D Changes in mitochondrial calcium levels in serum-starved WT and Nox4KO MEFs after the addition of histamine (100 μmol/L, C) or ATP (100 μmol/L, D). n=3/group (with >30 cells per individual experiment).

E, F Changes in ER calcium levels measured with an ER-targeted cameleon probe in serum-starved WT and Nox4KO MEFs after the addition of histamine (100 μmol/L, E) or ATP (100 μmol/L, F). n=3/group (with >30 cells per individual experiment).

G Peak increase in mitochondrial calcium levels response in response to histamine (100 μmol/L) in WT MEFs with or without treatment with PEG-catalase (Cat), and in Nox4KO MEFs with or without transfection with active Nox4 or a catalytically inactive Nox4P437H mutant (Mut). n=3/group (with >30 cells per individual experiment).

H Representative time-course of histamine-induced changes in mitochondrial calcium for the experiments shown in (I).

Data information: Data are mean ± SEM. ** P<0.01; **** P<0.0001 among compared groups or vs control. #### P<0.0001 vs Nox4KO. A, B: Student's t-test; C-H: 2-way repeated measures ANOVA; I: 1-way ANOVA