1 ig  (Proteintech)

Journal: bioRxiv

Article Title: YAP/TAZ-controlled ERK dynamics coordinate progenitor expansion and differentiation commitment

doi: 10.64898/2026.09.24.753950

Figure Lengend Snippet: (a) Immunofluorescence images of OP9 cells expressing endogenously tagged PPARG-mCitrine (green) and a nuclear marker (blue) before (0 h) and after 96 h of adipogenic differentiation. Scale bar, 50 µm. (b) Single-cell PPARG-mCitrine trajectories during adipogenic differentiation. Cells that crossed the PPARG commitment threshold are shown in green and uncommitted cells in gray. The dashed line indicates the commitment threshold. DMI was present for the first 48 h (bar). Right, distribution of PPARG levels at 96 h. (c) Schematic illustrating progenitor expansion before adipogenic differentiation commitment. Following an adipogenic stimulus, low-PPARG progenitors can undergo multiple divisions, expanding the population available for subsequent differentiation. Commitment occurs when PPARG crosses its threshold, after which cells proceed to the PPARG-high differentiated adipocyte state. (d) Design of the doxycycline-inducible, auxin-degradable constitutively active YAP and TAZ constructs (YAP-CA or TAZ-CA–mRuby3–mAID). Doxycycline induces construct expression, whereas auxin promotes degradation of the induced protein. (e) Experimental scheme used to validate reversible YAP-CA expression. Cells were treated with vehicle or doxycycline beginning on day 0. Expression was assessed on day 1. From day 1 to day 2, cells were maintained with vehicle or doxycycline, or auxin was added to doxycycline-treated cells while doxycycline was maintained. (f) Representative images of YAP-CA-mRuby3 (magenta) and nuclei (white) on days 1 and 2 for the indicated treatment conditions, showing low basal expression in control cells, induction by doxycycline, maintenance of expression with continued doxycycline, and loss of induced protein after auxin addition in the continued presence of doxycycline. (g) Experimental timeline for measuring proliferation and differentiation after YAP-CA or TAZ-CA induction. Cells were stimulated with DMI for 48 h. EdU was added for 15 min immediately before fixation on day 2. (h) Cells were treated with increasing doxycycline concentrations to generate a range of YAP-CA-S2A (left) or TAZ-CA-S2A (right) expression levels and binned according to nuclear mRuby3 fluorescence. Points show the mean percentage of PPARG-high cells (green, left axis) and EdU-positive cells (black, right axis) across two replicate wells for each expression bin. Data are representative of two independent experiments. (i) Total cell number (top) and percentage of PPARG-high cells (bottom) during 96 h of adipogenic differentiation after knockdown of YAP and TAZ together (siYAPTAZ), YAP alone (siYAP), or TAZ alone (siTAZ), compared with control siRNA (siCTRL). DMI was present for the first 48 h (bar). Line plots show mean ± 95% CI from three replicate wells per condition and are representative of two independent experiments. (j) Violin plots showing the distribution of single-cell nuclear YAP (left) and TAZ (right) fluorescence after the indicated siRNA treatments. Lines indicate the 25th, 50th, and 75th percentiles. At least 1,500 cells were analyzed per condition. Statistical significance was assessed by one-way ANOVA with Fisher’s LSD post-hoc test. All pairwise comparisons were performed against Ctrl siRNA condition, P < 0.0001.

Article Snippet: Primary antibodies were diluted in PBS containing 1% BSA and 0.3% Triton X-100 and incubated overnight at 4 °C: YAP (Cell Signaling Technology, D8H1X, cat. 14074, 1:1000), TAZ (Cell Signaling Technology, E8E9G, cat. 83669, 1:1000), PPARG (Santa Cruz Biotechnology, E-8, sc-7273, 1:1000), Pan-TEAD (Cell Signaling Technology, D3F7L, 1:1000), phospho-p44/42 MAPK (Thr202/Tyr204) (Cell Signaling Technology, 4370, 1:400), and total p44/42 MAPK (Cell Signaling Technology, 4696, 1:400).

Techniques: Immunofluorescence, Expressing, Marker, Single Cell, Construct, Control, Fluorescence, Knockdown

Journal: bioRxiv

Article Title: YAP/TAZ-controlled ERK dynamics coordinate progenitor expansion and differentiation commitment

doi: 10.64898/2026.09.24.753950

Figure Lengend Snippet: Unless otherwise indicated, cells were differentiated with DMI from day 0 to day 2, followed by insulin-containing medium without DMI from day 2 to day 4. (a) Yap1 and Wwtr1 (TAZ) mRNA levels (transcripts per million, TPM) measured by RNA-seq in OP9 cells over days 0–4 of adipogenic differentiation. Data are mean ± s.e.m. from three biologically independent samples per time point. (b) Total YAP protein (RFU) measured in single cells as the sum of nuclear (solid) and cytosolic (hatched) fractions by quantitative immunofluorescence over days 0–4 of adipogenesis. Bar plots show mean ± s.d. from 5 replicate wells; representative of two biologically independent experiments, ≥1,000 cells per experiment. (c) Mean nuclear-to-cytosolic ratio of YAP protein in single cells for data in . Bars show the overall means for each time point, and individual points show the means from replicate wells. (d) Mean YAP nuclear-to-cytosolic ratio from PPARG-high and PPARG-low cells at each time point. Day 0 contains no PPARG-high cells for data shown in . PPARG-high cells have significantly lower ratios than PPARG-low cells at all time points tested; Plotted as in . Multiple t-tests (Day 1, P = 0.0022; Day 2-4, P < 0.0001). (e) Total TAZ protein (RFU) measured in single cells as the sum of nuclear (solid) and cytosolic (hatched) fractions by quantitative immunofluorescence over days 0–4 of adipogenesis. Total TAZ increases over the time course, driven by cytosolic accumulation, while nuclear TAZ remains approximately unchanged. Bars show mean ± s.d. from 5 replicate wells; representative of two biologically independent experiments, ≥1,000 cells per experiment. (f) Mean TAZ nuclear-to-cytosolic ratio in single cells over days 0–4 for data shown in ; plotted as in . (g) TAZ nuclear-to-cytosolic ratio separated by PPARG level for data shown in ; plotted as in . (h) Tead1–Tead4 mRNA (TPM) measured by RNAseq analysis in unstimulated OP9 preadipocytes. Bars show the mean and points show the individual TPM values measured for three independent biological samples. (i) Combined Tead1–3 mRNA levels (TPM) over days 0–4 of adipogenic differentiation of OP9 cells. Plots show the mean ± s.e.m. of three biologically independent samples per time point. (j) Heatmap of log2 fold change relative to day 0 for canonical YAP/TAZ–TEAD target genes ( Ccn2(Ctgf), Amotl2 , Lox , Ccn1 (Cyr61) ) and extracellular-matrix genes in OP9 cells across days 0–4 of adipogenic differentiation measured by RNAseq. n = 3 biologically independent samples per time point. (k) Scheme showing two levels of YAP/TAZ–TEAD regulation: LATS1/2-dependent cytoplasmic redistribution reduces the active nuclear pool of YAP and TAZ, and declining TEAD expression limits transcriptional output; GNE-7883 blocks YAP/TAZ–TEAD-dependent transcription. (l) Expression of the canonical YAP/TAZ–TEAD target genes Amotl2 , Ccn1 (Cyr61) , Ccn2 (Ctgf) , and Lox after 24 h of GNE-7883 treatment (2.5 µM) or vehicle (DMSO), measured by qPCR and normalized to Gapdh . n = 3 independently treated biological samples, each measured in technical duplicate. Technical duplicates were averaged within each biological sample before statistical analysis. Bars show the mean and points indicate individual biological-sample 2^-ΔCq values. Unpaired two-tailed t -tests with Welch’s correction; Amotl2 , P = 0.0064; Ccn1 , P = 0.0007; Ccn2 , P = 0.0010; Lox , P = 0.0032.

Article Snippet: Primary antibodies were diluted in PBS containing 1% BSA and 0.3% Triton X-100 and incubated overnight at 4 °C: YAP (Cell Signaling Technology, D8H1X, cat. 14074, 1:1000), TAZ (Cell Signaling Technology, E8E9G, cat. 83669, 1:1000), PPARG (Santa Cruz Biotechnology, E-8, sc-7273, 1:1000), Pan-TEAD (Cell Signaling Technology, D3F7L, 1:1000), phospho-p44/42 MAPK (Thr202/Tyr204) (Cell Signaling Technology, 4370, 1:400), and total p44/42 MAPK (Cell Signaling Technology, 4696, 1:400).

Techniques: RNA Sequencing, Immunofluorescence, Analysis, Expressing, Two Tailed Test

Journal: bioRxiv

Article Title: YAP/TAZ-controlled ERK dynamics coordinate progenitor expansion and differentiation commitment

doi: 10.64898/2026.09.24.753950

Figure Lengend Snippet: (a) Experimental timeline. OP9 cells were transfected with siRNA and plated on day −1. Adipogenic differentiation was initiated with DMI on day 0, and cells were imaged continuously for 96 h, with a media refresh on day 2. DMI was maintained throughout the 96-h experiment. (b) Percentage of PPARG-high cells over time after treatment with control siRNA (siCTRL), combined YAP and TAZ siRNAs (siYAP + TAZ), or LATS1 siRNA (siLATS1). Line plots show mean ± s.e.m. from six replicate wells per condition. (c) Total number of PPARG-high cells over time for the conditions shown in b. Line plots show mean ± s.e.m. from six replicate wells per condition. (d–f) Single-cell analysis of PPARG accumulation, cell division, and differentiation commitment after treatment with siCTRL (d), siLATS1 (e), or siYAP + TAZ (f). Left and middle panels show representative single-cell traces of PPARG (blue, left axis) and integrated H2B signal (red, right axis). Abrupt decreases in integrated H2B signal mark cell divisions, and yellow circles indicate the time of differentiation commitment. Right, normalized frequency distributions of the number of divisions completed before differentiation commitment.

Article Snippet: Primary antibodies were diluted in PBS containing 1% BSA and 0.3% Triton X-100 and incubated overnight at 4 °C: YAP (Cell Signaling Technology, D8H1X, cat. 14074, 1:1000), TAZ (Cell Signaling Technology, E8E9G, cat. 83669, 1:1000), PPARG (Santa Cruz Biotechnology, E-8, sc-7273, 1:1000), Pan-TEAD (Cell Signaling Technology, D3F7L, 1:1000), phospho-p44/42 MAPK (Thr202/Tyr204) (Cell Signaling Technology, 4370, 1:400), and total p44/42 MAPK (Cell Signaling Technology, 4696, 1:400).

Techniques: Transfection, Control, Single-cell Analysis, Single Cell

Journal: bioRxiv

Article Title: YAP/TAZ-controlled ERK dynamics coordinate progenitor expansion and differentiation commitment

doi: 10.64898/2026.09.24.753950

Figure Lengend Snippet: (a) Experimental timeline and treatment conditions. OP9 cells expressing doxycycline-inducible, auxin-degradable YAP-CA or TAZ-CA constructs were plated on day −1 and stimulated with DMI from day 0 to day 3. Cells were treated with vehicle throughout (Control), doxycycline from day 0 to day 4 (Dox), or doxycycline from day 0 to day 1, after which doxycycline was removed and auxin was added from day 1 to day 4 (Dox and Aux). Cells were fixed on day 4. Doxycycline concentrations were 3 µg/mL for YAP-CA-S2A, 1 µg/mL for YAP-CA-S5A, and 0.25 µg/mL for TAZ-CA-S2A. (b) , (f) , (j) Representative images of PPARG (green) and nuclei (magenta) for Control, Dox, and Dox + Aux conditions for YAP-CA-S2A ( b ), YAP-CA-S5A ( f ), and TAZ-CA-S2A ( j ). Scale bar, 100 µm. (c) , (g) , (k) Total cell number for YAP-CA-S2A ( c ), YAP-CA-S5A ( g ), and TAZ-CA-S2A ( k ). (d) , (h) , (l) Number of PPARG-high cells for YAP-CA-S2A ( d ), YAP-CA-S5A ( h ), and TAZ-CA-S2A ( l ). (e) , (i) , (m) Percentage of PPARG-high cells for YAP-CA-S2A (e), YAP-CA-S5A (i), and TAZ-CA-S2A (m). For c–e, g–i, and k–m, bars show the mean and points indicate individual replicate wells, with five replicate wells per condition. Data are representative of two independent experiments. Statistical significance was assessed by one-way ANOVA followed by Dunnett’s multiple-comparisons test. Exact P values are shown in the figure; ns, not significant.

Article Snippet: Primary antibodies were diluted in PBS containing 1% BSA and 0.3% Triton X-100 and incubated overnight at 4 °C: YAP (Cell Signaling Technology, D8H1X, cat. 14074, 1:1000), TAZ (Cell Signaling Technology, E8E9G, cat. 83669, 1:1000), PPARG (Santa Cruz Biotechnology, E-8, sc-7273, 1:1000), Pan-TEAD (Cell Signaling Technology, D3F7L, 1:1000), phospho-p44/42 MAPK (Thr202/Tyr204) (Cell Signaling Technology, 4370, 1:400), and total p44/42 MAPK (Cell Signaling Technology, 4696, 1:400).

Techniques: Expressing, Construct, Control

Journal: bioRxiv

Article Title: YAP/TAZ-controlled ERK dynamics coordinate progenitor expansion and differentiation commitment

doi: 10.64898/2026.09.24.753950

Figure Lengend Snippet: (a) Working model and perturbation strategy used to distinguish the proliferative and differentiation-suppressive effects of YAP/TAZ. Mechanical inputs, including cell density and contact inhibition, act through AMOTL2/NF2/LATS to restrain YAP/TAZ–TEAD activity. YAP/TAZ–TEAD signaling promotes proliferation through AKT and CDK4/6 and suppresses differentiation through ERK. Pharmacological inhibitors used to perturb these pathways are indicated in color. (b), (c) Total YAP (in b ) and TAZ (in c ) levels (nuclear + cytosol) measured by quantitative immunofluorescence after 24 h treatment with TDI-011536 at the indicated concentrations versus untreated control. Bars show the overall means and data points show the individual means of 2-4 replicate wells per condition. n ≥ 1,000 cells per condition. (d) Percentage of EdU-positive cells after 24 h treatment with TDI-011536 at the indicated concentrations. Bars show the mean, and points indicate individual replicate-well means. (e) – (h) Dual-reporter OP9 cells expressing PPARG-mCitrine and an mCherry-APC/C cell-cycle reporter were stimulated with DMI and treated with vehicle (Ctrl), the LATS1/2 inhibitor TDI-011536 (LATSi), or LATSi together with the indicated pathway inhibitor: TEAD inhibitor GNE-7883 (e), CDK4/6 inhibitor palbociclib (f), MEK inhibitor PD-0325901 (g), or AKT inhibitor miransertib (h). Cells were imaged for 48 h. Left, total cell number. Right, percentage of PPARG-high cells. Lines show the mean and shaded regions indicate 95% confidence intervals across three replicate wells per condition. The Ctrl and LATSi traces are the same dataset in e–h and are repeated to facilitate comparison with each inhibitor condition. Inhibitor concentrations were 200 nM TDI-011536, 2.5 µM GNE-7883, 2.5 µM palbociclib, 200 nM PD-0325901, and 200 nM miransertib.

Article Snippet: Primary antibodies were diluted in PBS containing 1% BSA and 0.3% Triton X-100 and incubated overnight at 4 °C: YAP (Cell Signaling Technology, D8H1X, cat. 14074, 1:1000), TAZ (Cell Signaling Technology, E8E9G, cat. 83669, 1:1000), PPARG (Santa Cruz Biotechnology, E-8, sc-7273, 1:1000), Pan-TEAD (Cell Signaling Technology, D3F7L, 1:1000), phospho-p44/42 MAPK (Thr202/Tyr204) (Cell Signaling Technology, 4370, 1:400), and total p44/42 MAPK (Cell Signaling Technology, 4696, 1:400).

Techniques: Inhibition, Activity Assay, Immunofluorescence, Control, Expressing, Comparison

Journal: bioRxiv

Article Title: YAP/TAZ-controlled ERK dynamics coordinate progenitor expansion and differentiation commitment

doi: 10.64898/2026.09.24.753950

Figure Lengend Snippet: (a) Experimental timeline. Cells were stimulated with DMI in the presence of vehicle, the LATS1/2 inhibitor TDI-011536 (LATSi), or the MEK inhibitor PD-0325901 (MEKi) and imaged live for 48 h. Histograms show the distribution of PPARG levels at 48 h for each condition. (b) Design of the ERK kinase-translocation reporter (ERK-KTR). The reporter contains an ERK-responsive ELK1 substrate fused to nuclear localization and export sequences and mRuby3. ERK-dependent phosphorylation promotes nuclear export, such that the cytoplasmic-to-nuclear fluorescence ratio reports ERK activity. Representative images illustrate predominantly nuclear localization at low ERK activity and cytoplasmic localization at high ERK activity. Scale bar, 5 µm. (c) Population dynamics of PPARG (top) and ERK-KTR activity (bottom) during 48 h of adipogenic differentiation in control, LATSi (TDI-011536, 200 nM), and MEKi (PD-0325901, 200 nM) conditions. Thin lines show individual-cell trajectories. For PPARG, the bold line indicates the population average. For ERK-KTR, the bold line indicates the 75th percentile of the single-cell distribution. The dashed horizontal line indicates the threshold used to define the high-ERK state. (d) Representative single-cell PPARG (blue, top) and ERK-KTR (orange, bottom) trajectories from two cells per condition. PPARG accumulation occurs after cells transition away from sustained high ERK activity. (e) Left, single-cell PPARG levels plotted against ERK-KTR activity during the 30–36 h time window for control, LATSi, and MEKi conditions. The vertical dashed line indicates the ERK-KTR threshold used to define high ERK activity. Right, percentage of time points classified as high ERK during the same time window. Bars show the mean, and points indicate individual replicate wells (n = 5 wells per condition). Statistical significance was assessed by one-way ANOVA followed by Dunnett’s multiple-comparisons test, with each treatment compared with control. Exact P values are shown. (f) Experimental timeline for testing whether constitutive MEK activation can bypass loss of YAP/TAZ. OP9 PPARG-mCitrine cells expressing doxycycline-inducible HA-tagged constitutively active MEK1 (MEK-CA-HA) were transfected with control or YAP + TAZ siRNA 24 h before DMI stimulation. DMI was present for the first 48 h. Cells were treated with increasing doxycycline concentrations to generate a range of MEK-CA-HA expression levels and were fixed at 96 h for HA immunofluorescence and PPARG-mCitrine measurement. (g, h) Single-cell PPARG-mCitrine levels plotted against MEK-CA-HA expression at 96 h in control siRNA (g) and YAP + TAZ siRNA (h) conditions, with and without doxycycline. Horizontal dashed lines indicate the PPARG-high threshold, and vertical dashed lines indicate the threshold for induced MEK-CA-HA expression. (i) Cells from the doxycycline-treated conditions were binned according to MEK-CA-HA expression (0.5 log2 RFU bins), and mean PPARG levels were calculated for each bin. Points show the mean PPARG level across three replicate wells, with error bars indicating s.d., for control and YAP + TAZ siRNA conditions.

Article Snippet: Primary antibodies were diluted in PBS containing 1% BSA and 0.3% Triton X-100 and incubated overnight at 4 °C: YAP (Cell Signaling Technology, D8H1X, cat. 14074, 1:1000), TAZ (Cell Signaling Technology, E8E9G, cat. 83669, 1:1000), PPARG (Santa Cruz Biotechnology, E-8, sc-7273, 1:1000), Pan-TEAD (Cell Signaling Technology, D3F7L, 1:1000), phospho-p44/42 MAPK (Thr202/Tyr204) (Cell Signaling Technology, 4370, 1:400), and total p44/42 MAPK (Cell Signaling Technology, 4696, 1:400).

Techniques: Translocation Assay, Phospho-proteomics, Fluorescence, Activity Assay, Control, Single Cell, Activation Assay, Expressing, Transfection, Immunofluorescence

Journal: bioRxiv

Article Title: YAP/TAZ-controlled ERK dynamics coordinate progenitor expansion and differentiation commitment

doi: 10.64898/2026.09.24.753950

Figure Lengend Snippet: YAP/TAZ promote AKT- and ERK-dependent progenitor proliferation while maintaining cells in a high-ERK state that delays PPARG accumulation. As the progenitor population expands, we propose that increasing cell density and contact-dependent Hippo/LATS signaling progressively reduce YAP/TAZ activity, providing a slow negative-feedback mechanism that terminates the proliferative phase. Declining YAP/TAZ activity causes cells to spend less time at high ERK activity, allowing PPARG to accumulate and cells to commit to differentiation. Thus, YAP/TAZ couple expansion of the progenitor pool to the subsequent transition into differentiation through fast regulation of ERK signaling and slower density-dependent negative feedback.

Article Snippet: Primary antibodies were diluted in PBS containing 1% BSA and 0.3% Triton X-100 and incubated overnight at 4 °C: YAP (Cell Signaling Technology, D8H1X, cat. 14074, 1:1000), TAZ (Cell Signaling Technology, E8E9G, cat. 83669, 1:1000), PPARG (Santa Cruz Biotechnology, E-8, sc-7273, 1:1000), Pan-TEAD (Cell Signaling Technology, D3F7L, 1:1000), phospho-p44/42 MAPK (Thr202/Tyr204) (Cell Signaling Technology, 4370, 1:400), and total p44/42 MAPK (Cell Signaling Technology, 4696, 1:400).

Techniques: Activity Assay

Journal: Bioactive Materials

Article Title: A foam cell-targeted lipophagy restoration strategy stabilizes vulnerable atherosclerotic plaques

doi: 10.1016/j.bioactmat.2026.02.041

Figure Lengend Snippet: Schematic of the anti-atherosclerotic mechanism of OPN-HMCN@MLT. ( A ) The study commenced with the synthesis of mesoporous carbon nanospheres (MCN) functionalized with an OPN-binding peptide and hyaluronic acid to construct the OPN-HMCN nanoplatform. The OPN-binding peptide was designed to recognize OPN enriched in the extracellular matrix and on the surface of foam cells, thereby enabling selective accumulation in OPN-rich pathological regions. Following OPN recognition, OPN-HMCN@MLT undergoes CD44-dependent endocytosis. Melatonin (MLT), a lipid autophagy–promoting agent, was subsequently encapsulated within the nanocarrier to form OPN-HMCN@MLT. Firstly, the released MLT can bind to and upregulate the expression of PPARα and PPARγ, which then promote the expression of downstream genes (ABCA1, ABCG1, ACOX-1, and CTP1A) and trigger the lipophagy. ( B ) Subsequently, its lipophagy-enhancing effects, including ABCA1/G1-mediated cholesterol efflux and CTP1A/ACOX-1-mediated mitochondrial fatty acid oxidation, were studied to confirm the reversal of foam cell formation. ( C ) These effects eventually promote foam cells to reverse into macrophages. Abbreviations: MCN, mesoporous carbon nanoparticle; OPN, osteopontin; MLT, melatonin; LDL, low-density lipoprotein; ox-LDL, oxidized low-density lipoprotein; PA, Photoacoustic.

Article Snippet: To block nonspecific binding, membranes were incubated with 5% skim milk for 1 h. Thereafter, membranes were incubated overnight at 4 °C with primary antibodies against ABCA1, ABCG1, ACOX1, CPT1A, LC3 (ab192890, 1:2000, abcam), LAMP1 (84658-5-RR, 1:8000, Proteintech), PPARα (66826-1-Ig, 1:3000, Proteintech), PPARγ (66936-1-Ig, 1:10000, Proteintech), P62 (18420-1-AP, 1:10000, Proteintech), MCAD (55210-1-AP, 1:3000, Proteintech), LCAD (17526-1-AP, 1:10000, Proteintech), tubulin (80762-1-RR, 1:10000, Proteintech), GAPDH (60004-1-Ig, 1:50000, Proteintech), and β-actin (66009-1-Ig, 1:20000, Proteintech).

Techniques: Binding Assay, Construct, Expressing

Journal: Cell Death & Disease

Article Title: Adipogenic transdifferentiation reprograms EMT-high PDAC cells into a post-mitotic adipocyte-like state and limits metastasis

doi: 10.1038/s41419-026-08613-4

Figure Lengend Snippet: A Graphic scheme of adipogenic transdifferentiation induction protocol and microphotographs of control and transdifferentiated AsPC-1 cells at day 0, 3, 7, and 10; Rectangle dialog boxes magnify the field of view from the two groups. B Visualization of accumulated lipid droplets by oil red O staining in control and transdifferentiated AsPC-1 cells on day 10 after induction. Five random fields of view were used for quantification, values were presented as the mean ± SD ( n = 5 per group) and compared by Student’s t -test. C Relative mRNA expression levels (normalized to ACTB expression from the same individual sample) of adipocyte markers adiponectin, CEBPA, PPARG , and FABP4 in eight human pancreatic cell lines. Values were presented as the mean ± SD ( n = 3 per group) and compared by Student’s t -test. Abbreviation: SD Standard deviation.

Article Snippet: The following primary antibodies were used: polyclonal antibody against CEBPA (12968-1-AP, Proteintech, USA), polyclonal antibody against FABP4 (12801-1-AP, Proteintech), polyclonal antibody against PPARG (16643-1-AP, Proteintech), and recombinant antibody against Ki-67 (GB1514499, Servicebio, China).

Techniques: Control, Staining, Expressing, Standard Deviation

Journal: Cell Death & Disease

Article Title: Adipogenic transdifferentiation reprograms EMT-high PDAC cells into a post-mitotic adipocyte-like state and limits metastasis

doi: 10.1038/s41419-026-08613-4

Figure Lengend Snippet: Visualization and quantification of immunostaining of CEBPA ( A ), PPARG ( B ), and FABP4 ( C ) in control and transdifferentiated AsPC-1 cells on day 10. The protein expression levels were quantified by integrated intensity and positive area of five random fields of view. Values were presented as the mean ± SD ( n = 5 per group) and compared by Student’s t -test. D The protein expression levels of CEBPA and PPARG as adipogenesis markers and GAPDH as reference marker in AsPC-1. Abbreviation: SD standard deviation.

Article Snippet: The following primary antibodies were used: polyclonal antibody against CEBPA (12968-1-AP, Proteintech, USA), polyclonal antibody against FABP4 (12801-1-AP, Proteintech), polyclonal antibody against PPARG (16643-1-AP, Proteintech), and recombinant antibody against Ki-67 (GB1514499, Servicebio, China).

Techniques: Immunostaining, Control, Expressing, Marker, Standard Deviation

Journal: Cell Death & Disease

Article Title: Adipogenic transdifferentiation reprograms EMT-high PDAC cells into a post-mitotic adipocyte-like state and limits metastasis

doi: 10.1038/s41419-026-08613-4

Figure Lengend Snippet: A Schematic illustration of orthotopic PDAC models workflow. B , C Orthotopic PDAC samples collected from control and transdifferentiated groups. Tumors were outlined with yellow dashes. Tumor weight and tumor volume were presented as mean ± SD ( n = 5 per group) and compared by Student’s t -test. D Relative mRNA expression levels of adipogenesis markers (CEBPA, PPARG, FABP4, and adiponectin), EMT markers (E-cadherin and vimentin), and EMT-TFs (Snail1, Snail2, Twist1, Twist2, ZEB1, and ZEB2) in control and transdifferentiated groups. Values were presented as the mean ± SD ( n = 5 per group) and compared by Student’s t -test. E Volcano map of differentially expressed genes (DEGs) between control and transdifferentiated group ( n = 5 per group). F GO term analysis of DEGs based on gene counts showed significantly downregulated pathways in transdifferentiated group, indicating reduced angiogenesis, cellular response to cytokines, extracellular matrix organization, and cell migration. G BODIPY detection of lipid droplets in control and transdifferentiated groups from orthotopic PDAC samples. Tumors were outlined with white dashes; a representative view of fields was magnified and displayed in Fig. . Abbreviation: PDAC Pancreatic ductal adenocarcinoma, SD Standard deviation, EMT epithelial-mesenchymal transition, TF transcription factor; DEG differentially expressed genes, GO Gene ontology.

Article Snippet: The following primary antibodies were used: polyclonal antibody against CEBPA (12968-1-AP, Proteintech, USA), polyclonal antibody against FABP4 (12801-1-AP, Proteintech), polyclonal antibody against PPARG (16643-1-AP, Proteintech), and recombinant antibody against Ki-67 (GB1514499, Servicebio, China).

Techniques: Control, Expressing, Migration, Standard Deviation