Journal: bioRxiv

Article Title: Targeting Aberrant FGFR Signaling with Infigratinib Enhances the Efficacy of BTK/PI3K Inhibitors and Bendamustine in Lymphoma Cells

doi: 10.64898/2025.12.23.695986

Figure Lengend Snippet: A) Heatmap showing expression of FGFR1/3 and FGF2/9 across a panel of cell lines derived from MCL, ABC-DLBCL, and germinal center B-cell (GCB) DLBCL; heatmap is based on log2 CPM (counts per million). The scale ranges from low (-4, blue) to high (+4, red). Each horizontal represents the values for one cell line. B) Immunoblot for FGFR1 protein in a subset of selected cell lines and C) its protein quantification expressed as a ratio to SP53; data is the average with the second replicate shown in Supplementary Figure 1.

Article Snippet: The following primary antibodies were used in TBST 5% BSA buffer: FGFR1 mouse monoclonal (M19B2) (NB600-1287, Novus),Bek/FGFR2 mouse monoclonal (C-8) (sc-6930, Santa Cruz), FGFR3 mouse monoclonal (MAB766-100, ReD) and FGFR-4 mouse monoclonal (A-10) (sc-136988, Santa Cruz).

Techniques: Expressing, Derivative Assay, Western Blot

Journal: Nature Communications

Article Title: PLK1 inhibition exhibits strong anti-tumoral activity in CCND1 -driven breast cancer metastases with acquired palbociclib resistance

doi: 10.1038/s41467-020-17697-1

Figure Lengend Snippet: Characteristics of patients and PDX.

Article Snippet: Anti Phospho-Rb (Ser807/811) (D20B12) and anti FGFR1 (D8E4) were purchased from Cell Signalling (Rabbit Monoclonal #8516 and #9740) and respectively used at 1:400 and 1:200, after unmasking in citrate buffer pH6 for anti-Phopsho-Rb and in EDTA buffer pH8 for Anti FGFR1.

Techniques: Amplification, Adjuvant

Journal: Nature Communications

Article Title: PLK1 inhibition exhibits strong anti-tumoral activity in CCND1 -driven breast cancer metastases with acquired palbociclib resistance

doi: 10.1038/s41467-020-17697-1

Figure Lengend Snippet: a GSEA enrichment plots corresponding to hallmarks G2/M checkpoint. The analysis was performed on RNA from seven PDX and four primary breast tumours. NES normalised enrichment score, FDR: false discovery rate. b Heat map of gene expression changes in the G2 M hallmark. c Up-regulation of mitotic genes transcripts in bone metastasis derived PDX ( n = 9) as compared to patient’s primary tumours ( n = 4) (min to max whiskers plots with line indicating the median). d Clinical history of the patient corresponding to HBCx-137 PDX. The patient was diagnosed with ER + PR + breast cancer highly proliferating (Ki67 35%) at 52 year old. Lung and bone metastases were detected only 3 months after the start of adjuvant chemotherapy. She was treated by letrozole and triptorelin before vertebroplasty and PDX establishment. Immunohistochemistry analysis of Ki67 and PLK1 in primary breast tumour, bone metastasis and PDX (Ki67 H -score were 35%, 10% and 95% respectively, and PLK1 H -score were 6, 15 and 25%). Scale bar 50 μm. e Genomic profile of primary tumour, bone metastasis and PDX assessed by whole-exome sequencing. The three tumours carry focal amplification of FGFR1 , FGFR2 and CCND1 and CN gain of CCNE2 . FGFR1 expression has been validated by IHC in the HBCx-137 PDX (95% of positive cells). f In vivo targeting of HBCx-137 PDX by volasertib (10 mg/kg 4 times/week), palbociclib (75 mg/kg 5 days/week) and AZD4547 (12.5 mg/kg 5 days per week) in monotherapy and in combination with fulvestrant. n = 5 independent xenografts (control, fulvestrant, AZD4547, fulv. + AZD4547), n = 7 (volasertib), n = 8 (fulv.+vola), n = 9 (palbo, palbo + fulv.). Mean ± SD. Volasertib treated xenografts were monitored after end of treatment to detect tumour recurrence. Two xenografts relapsed at day 70 and 100 and were rechallenged with volasertib. g RT-PCR analysis of ER regulated genes ( TFF1 , GREB1 and PR ), ESR1 , PLK1 , Ki67 , PCNA and CENPE in treated tumours. Min-to-max whisker box plots with line indicating the median, n = 4 independent xenografts for all groups, with the exception of volasertib where n = 3 (xenografts were sacrificed before complete response for these xenografts). Source data from c and g are provided as a Source Data file.

Article Snippet: Anti Phospho-Rb (Ser807/811) (D20B12) and anti FGFR1 (D8E4) were purchased from Cell Signalling (Rabbit Monoclonal #8516 and #9740) and respectively used at 1:400 and 1:200, after unmasking in citrate buffer pH6 for anti-Phopsho-Rb and in EDTA buffer pH8 for Anti FGFR1.

Techniques: Gene Expression, Derivative Assay, Adjuvant, Immunohistochemistry, Sequencing, Amplification, Expressing, In Vivo, Control, Reverse Transcription Polymerase Chain Reaction, Whisker Assay

Journal: Nature Communications

Article Title: PLK1 inhibition exhibits strong anti-tumoral activity in CCND1 -driven breast cancer metastases with acquired palbociclib resistance

doi: 10.1038/s41467-020-17697-1

Figure Lengend Snippet: a clinical history, genomic profile and drug response of PDX HBCx-124. The HBCx-124 PDX was established from a patient diagnosed with metastatic BC at 26 years old. She was treated by chemotherapy (AC) and tamoxifen was given after the vertebroplasty. Copy number alterations in patients’ BC and PDX include amplification of CCND1 , CCNE2 , AURKA and FGFR1 . The PDX was treated by volasertib as compared to palbociclib ± fulvestrant. RTV = relative tumour volume. Mean ± SD ( n = 5 in control and fulvestrant treated groups; n = 7 in fulv. + vola., palbo, and palbo + fulv. treated groups; n = 8 in volasertib treated group). b Clinical history, genomic profile and drug response of the HBCx-131 PDX. The PDX was established from a patient diagnosed with breast cancer at 41 years old. The patient was treated by neo-adjuvant chemotherapy followed by mastectomy and adjuvant hormone-therapy (tamoxifen + anastrozole). She recurred with lung and bone metastasis 10 years later and was treated by letrozole. Patient’s tumour, bone met. and PDX carry amplification of CCND1 and FGFR1 . A homozygous deletion of CDKN2A/B emerged in bone metastasis (and PDX).The PDX was treated by volasertib as compared to palbociclib ± fulvestrant. Mean ± SD ( n = 6). c Clinical history, CNA profile and drug response of PDX HBCx-139. The PDX was established from a patient diagnosed with breast cancer at 33 years old, treated by neo-adjuvant chemotherapy and adjuvant tamoxifen. She recurred 10 years later with liver and bone metastases and was treated by different lines of chemotherapies and everolimus. The genomic profile of HBCx-139 PDX was analysed by cytoscan HD array: the PDX carry amplification of PAK1 and has CN gains for CCND1 , CDK7 and CCNB1 . The PDX is also PIK3CA mutated and was treated by volasertib as compared to palbociclib and the PI3Kα inhibitor alpelisib (BYL-719) ± fulvestrant. RTV relative tumour volume. Mean ± SD ( n = 5 in control group, n = 6 in fulvestrant, palbo treated group, n = 7 in volasertib, volasertib + fulv., alpelisib and alpelisib + fulv.).

Article Snippet: Anti Phospho-Rb (Ser807/811) (D20B12) and anti FGFR1 (D8E4) were purchased from Cell Signalling (Rabbit Monoclonal #8516 and #9740) and respectively used at 1:400 and 1:200, after unmasking in citrate buffer pH6 for anti-Phopsho-Rb and in EDTA buffer pH8 for Anti FGFR1.

Techniques: Amplification, Control, Adjuvant

Journal: Theranostics

Article Title: Peptide ligands targeting FGF receptors promote recovery from dorsal root crush injury via AKT/mTOR signaling

doi: 10.7150/thno.62525

Figure Lengend Snippet: Role of FGFR signaling in response to the CH02 peptide on promoting nerve regeneration. (A) Western blot analysis of phosphorylated FGFR expression in C5-T1 DRGs subjected to dorsal root crush injury, followed by CH02 treatment (20 μM). DRGs were collected after 3 days. Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) antibodies were used as the loading control. (B) Western blot analysis of phosphorylated FGFR expression in ex vivo cultured DRG explants of adult Sprague-Dawley rats in response to CH02 treatment at different induction times. (C) Western blot analysis of DRG explants treated with DMSO (control), CH02 (20 μM), CH02+BGJ398, or BGJ398 (2 μM) for 4 h to examine phospho-FGFR levels after 6 days in ex vivo culture. Tubulin antibodies were used as the loading control. (D-F) Quantification of p-FGFR expression levels in panels A, B, and C. n = 3 independent experiments. Relative protein expression levels were quantified after normalization to FGFR2 or FGFR1. Values are means ± SEM. (G) Representative images of the CH02 effect on axonal growth in ex vivo DRG explants cultured for 1 day and treated with DMSO (control), CH02 (20 μM), CH02+BGJ398, or BGJ398 (2 μM) for 4 days. DRG explants were fixed in 4% paraformaldehyde and immunostained for NF200 antibodies. Scale bar = 100 μm. (H) Quantification of axon growth in DRG explants (G) using Neurite-J software (n = 5 for each condition; *control vs. CH02; #control vs. BGJ398; ** p < 0.01, *** p < 0.001, **** p < 0.0001, # p < 0.05, ## p < 0.01 by two-way ANOVA with Dunnett's test; mean ± SEM). (I) Representative images of the CH02 effect on axonal growth in primary cultured DRG neurons treated with DMSO (control), CH02 (20 μM), CH02+BGJ398, orBGJ398 (2 μM) for 48 h after 12- h of culture. Subsequently, DRG neurons were fixed in 4% paraformaldehyde and immunostained with β-tubulin antibodies. Images of random neurons were acquired by fluorescence microscopy. Scale bar = 25 μm. (J) Quantification of the longest axon length of each neuron randomly selected from (I) using Image-Pro Plus 6.0 software (n = 100 for each condition; * p < 0.05, ** p < 0.01, **** p < 0.0001 by one-way ANOVA with Dunnett's; ns, not significant; mean ± SD).

Article Snippet: The primary antibodies used were as follows: rabbit polyclonal anti-phospho-FGFR (1:1000; CST); anti-FGFR2 (1:1000; Abcam), rabbit monoclonal anti-FGFR1(1:1000; CST), rabbit monoclonal anti-phospho-VEGFR2 (1:1000; CST), rabbit monoclonal anti-VEGFR2 (1:1000; CST), rabbit polyclonal anti-phospho-ERBB2 (1:1000; Abcam), rabbit monoclonal anti-ERBB2 (1:1000; Abcam), rabbit monoclonal anti-phospho-MET (1:1000; CST), rabbit monoclonal anti-MET (1:1000; Abcam), rabbit monoclonal anti-phospho- PDGFR beta (1:1000; Abcam), rabbit monoclonal anti-PDGFR beta (1:1000; Abcam), rabbit monoclonal anti-phospho-ERK1/2 (1:1000; CST), rabbit monoclonal anti-ERK1/2 (1:1000; CST), rabbit monoclonal anti-phospho-AKT (1:1000; CST), rabbit monoclonal anti-AKT (1:1000; CST), rabbit monoclonal anti-mTOR (1:1000; CST), rabbit monoclonal anti-phospho-mTOR (1:1000; CST), rabbit monoclonal anti-β-Tubulin (1:1000; CST), and rabbit monoclonal anti- GAPDH (1:1000; CST).

Techniques: Western Blot, Expressing, Control, Ex Vivo, Cell Culture, Software, Fluorescence, Microscopy

Journal: Oxidative Medicine and Cellular Longevity

Article Title: DJ-1/FGFR-1 Signaling Pathway Contributes to Sorafenib Resistance in Hepatocellular Carcinoma

doi: 10.1155/2022/2543220

Figure Lengend Snippet: DJ-1 induced FGFR1 phosphorylation and activated the Akt, ERK, and STAT signaling pathways in ECDHCC-1 cells. (a and b) Cells were treated with DJ-1 (15 μ g/mL) for 24 h, and then the mRNA expression of FGFR1 (a) and protein expression of phosphorylated FGFR1 (p-FGFR1) and total FGFR1 (b) were detected by qRT-PCR and western blotting analysis, respectively. The inducing activity of DJ-1 was compared with that of EGF (20 ng/mL). (c) Co-immunoprecipitation assay for FGFR1 and DJ-1 was performed. (d–g) Western blotting analysis of Akt, mTOR, ERK, and STAT3 phosphorylation was conducted. The inducing activity of DJ-1 was compared with that of EGF (20 ng/mL). ∗ P < 0.05 and ∗∗ P < 0.01 versus Con.

Article Snippet: Our primary antibodies are listed below: p-FGFR1-Tyr653/654 mouse mAb (#3476, 1 : 500, CST, USA), FGFR1 mouse mAb (#60325-1-Ig, 1 : 1000, Proteintech, USA), p-Akt-S473 rabbit pAb (#AP0140, 1 : 1000, ABclonal, China), Akt rabbit pAb (#11016, 1 : 1000, ABclonal, China), p-mTOR-S2448 rabbit pAb (#AP0094, 1 : 1000, ABclonal, China), mTOR rabbit pAb (#20657-1-AP, 1 : 1000, Proteintech, USA), p-ERK1/2 (ERK1-T202/Y204+ERK2-T185/Y187) rabbit pAb (#AP0472, 1 : 1000, ABclonal, China), ERK1/2 rabbit pAb (#16443-1-AP, 1 : 1000, Proteintech, USA), p-STAT3- Tyr705 rabbit pAb (#381552, 1 : 1000, ZEN, China), STAT3 rabbit pAb (#A11216, 1 : 1000, ABclonal, China), cleaved caspase 3 rabbit pAb (#A2156, 1 : 1000, ABclonal, China), cleaved caspase 9 rabbit pAb (#A2636, 1 : 1000, ABclonal, China), Bax rabbit pAb (#50599-2-Ig, 1 : 1000, Proteintech, USA), Bcl-2 rabbit pAb (#12789-1-AP, 1 : 1000, Proteintech, USA), and GAPDH rabbit mAb (#2118S, 1 : 1000, CST, USA).

Techniques: Phospho-proteomics, Protein-Protein interactions, Expressing, Quantitative RT-PCR, Western Blot, Activity Assay, Co-Immunoprecipitation Assay

Journal: Oxidative Medicine and Cellular Longevity

Article Title: DJ-1/FGFR-1 Signaling Pathway Contributes to Sorafenib Resistance in Hepatocellular Carcinoma

doi: 10.1155/2022/2543220

Figure Lengend Snippet: Downregulation of FGFR1 inhibited tube formation and migration of ECDHCC-1 cells stimulated by DJ-1. (a) and (b) Knockdown of FGFR1 by shRNA was confirmed by qRT-PCR and western blotting analysis. (c) Cell viability was analyzed by CCK8. (d–f) The effect of FGFR1 knockdown on DJ-1 inducing angiogenesis on EDCHCC-1 cells was assessed for tube formation assay (d), the number of nodes (e), and total length (f) of capillary tube. n = 3 for all groups. (g) and (h) The effect of FGFR1 knockdown on DJ-1 inducing migration on EDCHCC-1 cells was examined. Photographs (×20) were taken at 12, 24, and 36 h, respectively, after treatment with 15 μ g/mL DJ-1 (g). Relative scratch width was quantified by image J software (h). ∗ P < 0.05 and ∗∗ P < 0.01 versus Con. (original magnifications: ×200 for fluorescence).

Article Snippet: Our primary antibodies are listed below: p-FGFR1-Tyr653/654 mouse mAb (#3476, 1 : 500, CST, USA), FGFR1 mouse mAb (#60325-1-Ig, 1 : 1000, Proteintech, USA), p-Akt-S473 rabbit pAb (#AP0140, 1 : 1000, ABclonal, China), Akt rabbit pAb (#11016, 1 : 1000, ABclonal, China), p-mTOR-S2448 rabbit pAb (#AP0094, 1 : 1000, ABclonal, China), mTOR rabbit pAb (#20657-1-AP, 1 : 1000, Proteintech, USA), p-ERK1/2 (ERK1-T202/Y204+ERK2-T185/Y187) rabbit pAb (#AP0472, 1 : 1000, ABclonal, China), ERK1/2 rabbit pAb (#16443-1-AP, 1 : 1000, Proteintech, USA), p-STAT3- Tyr705 rabbit pAb (#381552, 1 : 1000, ZEN, China), STAT3 rabbit pAb (#A11216, 1 : 1000, ABclonal, China), cleaved caspase 3 rabbit pAb (#A2156, 1 : 1000, ABclonal, China), cleaved caspase 9 rabbit pAb (#A2636, 1 : 1000, ABclonal, China), Bax rabbit pAb (#50599-2-Ig, 1 : 1000, Proteintech, USA), Bcl-2 rabbit pAb (#12789-1-AP, 1 : 1000, Proteintech, USA), and GAPDH rabbit mAb (#2118S, 1 : 1000, CST, USA).

Techniques: Migration, Knockdown, shRNA, Quantitative RT-PCR, Western Blot, Tube Formation Assay, Software, Fluorescence

Journal: Oxidative Medicine and Cellular Longevity

Article Title: DJ-1/FGFR-1 Signaling Pathway Contributes to Sorafenib Resistance in Hepatocellular Carcinoma

doi: 10.1155/2022/2543220

Figure Lengend Snippet: Downregulation of FGFR1 attenuated the phosphorylation of FGFR1 and reversed the activity of Akt, ERK, and STAT3 signal induced by DJ-1. Cells with stable knockdown of FGFR1 were treated with or without DJ-1 (15 μ g/mL) for 24 h, and then, the protein expression of p-FGFR1/FGFR1 (a), p-Akt/Akt (b), p-mTOR/mTOR (c), p-ERK1/2/ERK1/2 (d), and p-STAT3/STAT3 (e) was examined by western blotting, respectively. The empty vector group was used as the control (Con). ∗ P < 0.05 and ∗∗ P < 0.01 versus Con.

Article Snippet: Our primary antibodies are listed below: p-FGFR1-Tyr653/654 mouse mAb (#3476, 1 : 500, CST, USA), FGFR1 mouse mAb (#60325-1-Ig, 1 : 1000, Proteintech, USA), p-Akt-S473 rabbit pAb (#AP0140, 1 : 1000, ABclonal, China), Akt rabbit pAb (#11016, 1 : 1000, ABclonal, China), p-mTOR-S2448 rabbit pAb (#AP0094, 1 : 1000, ABclonal, China), mTOR rabbit pAb (#20657-1-AP, 1 : 1000, Proteintech, USA), p-ERK1/2 (ERK1-T202/Y204+ERK2-T185/Y187) rabbit pAb (#AP0472, 1 : 1000, ABclonal, China), ERK1/2 rabbit pAb (#16443-1-AP, 1 : 1000, Proteintech, USA), p-STAT3- Tyr705 rabbit pAb (#381552, 1 : 1000, ZEN, China), STAT3 rabbit pAb (#A11216, 1 : 1000, ABclonal, China), cleaved caspase 3 rabbit pAb (#A2156, 1 : 1000, ABclonal, China), cleaved caspase 9 rabbit pAb (#A2636, 1 : 1000, ABclonal, China), Bax rabbit pAb (#50599-2-Ig, 1 : 1000, Proteintech, USA), Bcl-2 rabbit pAb (#12789-1-AP, 1 : 1000, Proteintech, USA), and GAPDH rabbit mAb (#2118S, 1 : 1000, CST, USA).

Techniques: Phospho-proteomics, Activity Assay, Knockdown, Expressing, Western Blot, Plasmid Preparation, Control

Journal: Oxidative Medicine and Cellular Longevity

Article Title: DJ-1/FGFR-1 Signaling Pathway Contributes to Sorafenib Resistance in Hepatocellular Carcinoma

doi: 10.1155/2022/2543220

Figure Lengend Snippet: Downregulation of FGFR1 affected the apoptosis of sorafenib-resistant HCC cells. (a) Cell viability of THLE-2, HepG2, and HUH-7 after treatment with indicated concentration of sorafenib was assessed by CCK8 assay, and half-maximal inhibitory concentration (IC 50 ) was calculated with a linear fit. (b) Sorafenib-resistant HUH-7 cell line (HUH-7/R) was constructed, and the cell viability was assessed to define the resistance index (RI) of the HUH-7/R cell line. (c) Western blotting analysis of multidrug resistance marker of P-gp and MRP1 was detected. (d and e) Flow cytometry assessment of cell apoptosis by annexin-V/PI (d) and two representative groups after transient knockdown of FGFR1 in HUH-7 and HUH-7/R cells was statistically analyzed (e). (f)–(l) Western blotting analysis of p-FGFR1/FGFR1, cleaved caspase 3, cleaved caspase 9, Bax, and Bcl-2 was carried out in HUH-7 and HUH-7/R cells after transient knockdown of FGFR1 and combined treatment with sorafenib and DJ-1. NS: Not significant, ∗ P < 0.05 versus DJ-1 group, and ∗∗ P < 0.01 versus the vehicle or DJ-1 alone.

Article Snippet: Our primary antibodies are listed below: p-FGFR1-Tyr653/654 mouse mAb (#3476, 1 : 500, CST, USA), FGFR1 mouse mAb (#60325-1-Ig, 1 : 1000, Proteintech, USA), p-Akt-S473 rabbit pAb (#AP0140, 1 : 1000, ABclonal, China), Akt rabbit pAb (#11016, 1 : 1000, ABclonal, China), p-mTOR-S2448 rabbit pAb (#AP0094, 1 : 1000, ABclonal, China), mTOR rabbit pAb (#20657-1-AP, 1 : 1000, Proteintech, USA), p-ERK1/2 (ERK1-T202/Y204+ERK2-T185/Y187) rabbit pAb (#AP0472, 1 : 1000, ABclonal, China), ERK1/2 rabbit pAb (#16443-1-AP, 1 : 1000, Proteintech, USA), p-STAT3- Tyr705 rabbit pAb (#381552, 1 : 1000, ZEN, China), STAT3 rabbit pAb (#A11216, 1 : 1000, ABclonal, China), cleaved caspase 3 rabbit pAb (#A2156, 1 : 1000, ABclonal, China), cleaved caspase 9 rabbit pAb (#A2636, 1 : 1000, ABclonal, China), Bax rabbit pAb (#50599-2-Ig, 1 : 1000, Proteintech, USA), Bcl-2 rabbit pAb (#12789-1-AP, 1 : 1000, Proteintech, USA), and GAPDH rabbit mAb (#2118S, 1 : 1000, CST, USA).

Techniques: Concentration Assay, CCK-8 Assay, Construct, Western Blot, Marker, Flow Cytometry, Knockdown

Journal: Oxidative Medicine and Cellular Longevity

Article Title: DJ-1/FGFR-1 Signaling Pathway Contributes to Sorafenib Resistance in Hepatocellular Carcinoma

doi: 10.1155/2022/2543220

Figure Lengend Snippet: FGFR1 knockdown impairs tumor growth and angiogenesis of sorafenib-resistant HCC cells in vivo. (a and b) Pilot studies of tumor xenograft experiments were performed for HUH-7/R cells with 3 groups of treatment: i.e., vehicle control; sorafenib+DJ-1; and sorafenib+DJ-1+shFGFR1. 5 × 10 6 cells per injection were injected subcutaneously into two flanks of nude mice ( n = 3), and tumor weight (a) and tumor volume (b) were recorded. Tumor volume was checked twice to three times weekly using a digital caliper. (c and d) Tumor cell angiogenesis was examined in the chicken chorioallantoic membrane (CAM) model. Both HUH-7 and HUH-7/R cells were mixed with ECDHCC-1 cells at the ratio of 1 : 1 and then treated at different conditions: (1) cells+control; (2) cells+DJ-1; (3) cells+corafenib; (4) cells+sorafenib+DJ-1; and (5) cells+sorafenib+DJ-1+shFGFR1. In CAM model, total vessel length (c) and density (d) were measured at the end of the experiments.

Article Snippet: Our primary antibodies are listed below: p-FGFR1-Tyr653/654 mouse mAb (#3476, 1 : 500, CST, USA), FGFR1 mouse mAb (#60325-1-Ig, 1 : 1000, Proteintech, USA), p-Akt-S473 rabbit pAb (#AP0140, 1 : 1000, ABclonal, China), Akt rabbit pAb (#11016, 1 : 1000, ABclonal, China), p-mTOR-S2448 rabbit pAb (#AP0094, 1 : 1000, ABclonal, China), mTOR rabbit pAb (#20657-1-AP, 1 : 1000, Proteintech, USA), p-ERK1/2 (ERK1-T202/Y204+ERK2-T185/Y187) rabbit pAb (#AP0472, 1 : 1000, ABclonal, China), ERK1/2 rabbit pAb (#16443-1-AP, 1 : 1000, Proteintech, USA), p-STAT3- Tyr705 rabbit pAb (#381552, 1 : 1000, ZEN, China), STAT3 rabbit pAb (#A11216, 1 : 1000, ABclonal, China), cleaved caspase 3 rabbit pAb (#A2156, 1 : 1000, ABclonal, China), cleaved caspase 9 rabbit pAb (#A2636, 1 : 1000, ABclonal, China), Bax rabbit pAb (#50599-2-Ig, 1 : 1000, Proteintech, USA), Bcl-2 rabbit pAb (#12789-1-AP, 1 : 1000, Proteintech, USA), and GAPDH rabbit mAb (#2118S, 1 : 1000, CST, USA).

Techniques: Knockdown, In Vivo, Control, Injection, Membrane

Journal: Investigative Ophthalmology & Visual Science

Article Title: Goblet Cell Differentiation Potential in Human Corneal Limbal Epithelial Progenitor Cells In Vitro

doi: 10.1167/iovs.61.12.27

Figure Lengend Snippet: FGFR, Fibroblast Growth Factor Receptor

Article Snippet: The following Abs were used: mouse anti-cytokeratin-3/2p monoclonal antibody (mAb; AE-5, 1:100; Santa Cruz Biotechnology, Inc, Dallas, TX, USA), mouse anti-human cytokeratin-4 mAb (6B10, 1:300; Abcam, Cambridge, UK), rabbit monoclonal [EP1599Y] anti-human cytokeratin 4 (1:200, Abcam), mouse anti-human cytokeratin-7 mAb (RCK105, 1:10000; Millipore, Billerica, MA, USA), mouse anti-human cytokeratin-13 mAb (1:20; American Research Products, Inc., Palos Verdes, CA, USA), mouse anti-human cytokeratin-12 mAb (N-16; 1:500; Santa Cruz Biotechnology), rabbit anti-cytokeratin 12/K12 mAb (1:200, EPR17882, Abcam), rabbit anti-human MUC5AC polyclonal Ab (H-160, 1:100, Santa Cruz Biotechnology), anti-FGFR1 mAb (1:200, 133105; R&D Systems, Minneapolis, MN, USA), anti-human FGFR2 (blocking) mAb (1:200, 98725; R&D Systems), anti-FGFR3 mAb (1:200, 135334; R&D Systems), anti-FGFR4 mAb (1:200, 137114; R&D Systems), and anti-FGFR1 blocking mAb (VBS1; Chemicon, Temecula, CA, USA).

Techniques:

Journal: Investigative Ophthalmology & Visual Science

Article Title: Goblet Cell Differentiation Potential in Human Corneal Limbal Epithelial Progenitor Cells In Vitro

doi: 10.1167/iovs.61.12.27

Figure Lengend Snippet: FGF receptor expression and effect of FGF receptor blockade in colonies derived from adherent single cells. ( A ) FGFR1 and FGFR2, but not FGFR3 and FGFR4, are detected in the adherent colonies by RT-PCR. ( B ) FGFR1 and FGFR2 expression is detected by Western blotting. ( C ) Effect of FGF receptor blockade was tested in colonies derived from adherent single cells. PAS-positive colony number in the anti-FGFR1 monoclonal antibody group significantly decreases as compared with that in the control Ig group. Treatment with an anti-FGFR2 blocking mAb does not affect the number of colony. ( D ) Colony with amorphous material and epithelium is observed with control IgG. ( E ) Anti-FGFR1 mAb suppresses the proliferation of both goblet-like cell and epithelium. Similar results were obtained with repeated three experiments. M, size markers; S, sample; P, positive control; N, negative control, N.S., not significant.

Article Snippet: The following Abs were used: mouse anti-cytokeratin-3/2p monoclonal antibody (mAb; AE-5, 1:100; Santa Cruz Biotechnology, Inc, Dallas, TX, USA), mouse anti-human cytokeratin-4 mAb (6B10, 1:300; Abcam, Cambridge, UK), rabbit monoclonal [EP1599Y] anti-human cytokeratin 4 (1:200, Abcam), mouse anti-human cytokeratin-7 mAb (RCK105, 1:10000; Millipore, Billerica, MA, USA), mouse anti-human cytokeratin-13 mAb (1:20; American Research Products, Inc., Palos Verdes, CA, USA), mouse anti-human cytokeratin-12 mAb (N-16; 1:500; Santa Cruz Biotechnology), rabbit anti-cytokeratin 12/K12 mAb (1:200, EPR17882, Abcam), rabbit anti-human MUC5AC polyclonal Ab (H-160, 1:100, Santa Cruz Biotechnology), anti-FGFR1 mAb (1:200, 133105; R&D Systems, Minneapolis, MN, USA), anti-human FGFR2 (blocking) mAb (1:200, 98725; R&D Systems), anti-FGFR3 mAb (1:200, 135334; R&D Systems), anti-FGFR4 mAb (1:200, 137114; R&D Systems), and anti-FGFR1 blocking mAb (VBS1; Chemicon, Temecula, CA, USA).

Techniques: Expressing, Derivative Assay, Reverse Transcription Polymerase Chain Reaction, Western Blot, Control, Blocking Assay, Positive Control, Negative Control