p ddr1 2  (R&D Systems)

Journal: Cancer Cell International

Article Title: PHI-501, a dual inhibitor of RAF and DDR1/2, overcomes MAPK drug resistance in Melanoma

doi: 10.1186/s12935-026-04271-w

Figure Lengend Snippet: MAPK inhibitor-resistant melanoma cells exhibit enhanced DDR1/2 signaling. ( A ) Clonogenic assay showing the validation of drug-resistant cell lines. ( B ) Quantification of clonogenic assay shown in Fig. 1A. Data are presented as relative colony formation (%) normalized to the control group and expressed as the mean ± SEM, n = 3 replicates. Statistical significance was determined by two-way ANOVA. * p < 0.05, # p < 0.001, † p < 0.001, ‡ p < 0.0001. ( C ) Cell viability assay of RAF and MEK inhibitors in parental cells and drug-resistant cells for 48 h. Data are presented as the mean ± SEM, n = 3 replicates. ( D ) Western blot analysis of pERK and pAKT signaling responses in parental and resistant melanoma cells following 48-h treatment with vehicle or the corresponding resistance-selecting drug(s) at 1 µM. ( E ) Bubble plot representing Gene Set Enrichment Analysis (GSEA) using hallmark gene set comparing parental and resistant melanoma cells. Pathway enrichment was calculated using GSEA, with color indicating NES (blue = downregulated, red = upregulated) and bubble size representing −log10(p-value). ( F ) SK-MEL-2 and SK-MEL-2BR cells were stimulated with type I collagen (40 µg/ml) for 18 h to activate DDR signaling

Article Snippet: The membranes were incubated overnight at 4 °C with primary antibodies diluted in 5% BSA in TBST as indicated in the text: p-DDR1 (Cell Signaling Technology, CST14531 ), p-DDR1/2 (R&D Systems, MAB25382), p-AKT (Cell Signaling Technology, CST4058), AKT (Cell Signaling Technology, CST9272), p-MEK (Cell Signaling Technology, CST9121), p-ERK (Cell Signaling Technology, CST9101), ERK (Cell Signaling Technology, CST9102), Cyclin D1(Cell Signaling Technology, CST2978), and Survivin (Cell Signaling Technology, CST2808).

Techniques: Clonogenic Assay, Biomarker Discovery, Control, Viability Assay, Western Blot

Journal: Cancer Cell International

Article Title: PHI-501, a dual inhibitor of RAF and DDR1/2, overcomes MAPK drug resistance in Melanoma

doi: 10.1186/s12935-026-04271-w

Figure Lengend Snippet: DDR1 and DDR2 are associated with MAPK pathway activation and therapeutic resistance in melanoma. ( A ) Kaplan–Meier survival analysis showing patient outcomes based on DDR1 and DDR2 expression levels across all TCGA cancer types. Patients were stratified into high (top 25%) and low (bottom 25%) expression groups, and overall survival (OS) was analyzed. ( B ) Proteomic analysis of BRAF/NRAS-mutant SKCM. Box plots demonstrate differential expression of AKT and phosphorylated MEK1 (pMEK1-S217/S221) between wild-type and mutant groups. ( C ) Correlation heatmaps between DDR1/2 and key genes in the MAPK and AKT signaling pathways in TCGA-SKCM samples. Color intensity represents the correlation value, with red indicating a positive correlation. Significance levels are indicated by asterisks (* p < 0.05, ** p < 0.01, *** p < 0.001). ( D ) Correlation analysis revealing DDR1 expression (DepMap) and MAPK pathway inhibitor sensitivity (GDSC2) in melanoma cell lines. Scatter plots depicting correlations between DDR1 expression levels and IC50 to Dabrafenib (left) and Trametinib (right)

Article Snippet: The membranes were incubated overnight at 4 °C with primary antibodies diluted in 5% BSA in TBST as indicated in the text: p-DDR1 (Cell Signaling Technology, CST14531 ), p-DDR1/2 (R&D Systems, MAB25382), p-AKT (Cell Signaling Technology, CST4058), AKT (Cell Signaling Technology, CST9272), p-MEK (Cell Signaling Technology, CST9121), p-ERK (Cell Signaling Technology, CST9101), ERK (Cell Signaling Technology, CST9102), Cyclin D1(Cell Signaling Technology, CST2978), and Survivin (Cell Signaling Technology, CST2808).

Techniques: Activation Assay, Expressing, Mutagenesis, Quantitative Proteomics, Protein-Protein interactions

Journal: eLife

Article Title: Control of craniofacial development by the collagen receptor, discoidin domain receptor 2

doi: 10.7554/elife.77257

Figure Lengend Snippet: Figure 1. Ddr2 deficiency results in impaired anterior-posterior skull growth with abnormal frontal bone and suture formation. WT and Ddr2slielsile mice were compared at 3 months (a–g) and 2 weeks (h,i). (a-c) Short snout, and reduced skull length in Ddr2slielsile mice. (a) Side (upper) and top (lower) head views of 3-month-old Ddr2slie/slie mice and WT littermates. Scale bar: 1 cm. (b) 3D rendering of μCT scans of 3-month-old skulls. Scale bar: 1 mm. (c) Linear measurements along anteroposterior axis of skulls, where SL: skull length; NB: nasal bone; CV: calvaria vault; ACB: anterior cranial base; PCB: posterior cranial base. (d) Quantification of anterior (ant.) and posterior (post.) skull width showed a selective increase only in the anterior skull of Ddr2slie/slie vs WT mice. (e) No changes were observed in skull height at any of the regions measured (anterior cranial height, ACH; middle cranial height, MCH; posterior cranial height, PCH). (f,g) μCT scans of calvarial bones and quantification showing a significant reduction of frontal bone (blue) in 3-month-old Ddr2slie/slie mice in the absence of changes in parietal (orange) or occipital (green) calvarial bones. Note frontal suture defect in Ddr2slie/

Article Snippet: After blocking, the sections were incubated at 4 °C overnight, with the following primary antibodies: anti- DDR2 (LS B15752, 1:200), anti- Y740- P- DDR2 (R&D Systems MAB25382, 1:200), anti- cleaved caspase 3 (Cell Signaling 9661, 1:200), anti- COL2 (Abcam ab34712, 1:100); anti- COL10 (Abcam ab58632, 1:100); Anti- COL1(Millipore Sigma AB765P, 1:100); Anti- GM130 (BD Biosciences 610822,1:100); anti- IBSP (1:100).

Techniques:

Journal: eLife

Article Title: Control of craniofacial development by the collagen receptor, discoidin domain receptor 2

doi: 10.7554/elife.77257

Figure Lengend Snippet: Figure 2. Cranial base hypoplasia due to chondrocyte disorganization and reduced chondrocyte proliferation in Ddr2-knockout synchondroses. (a) H&E staining (upper) and μCT scans (lower) of WT and Ddr2slie/slie skulls showing wide cranial base synchondroses. Scale bar: 500 μm. Boxed region (red) is shown in higher magnification. Br: Brain; t: Tongue. ISS: Intersphenoid synchondrosis; SOS: Spheno-occipital synchondrosis; PS: Presphenoid bone; BS: Basisphenoid bone; BO: Basis-occipital bone. In μCT scan of skulls (lower), arrowheads point to cranial base synchondroses; yellow and red lines highlight the width and height of synchondroses; respectively (Quantification is shown in b). Cyan lines highlight shortening of basisphenoid bone between ISS and SOS in Ddr2slie/slie vs WT mice (Quantification of cranial base bone lengths is shown in c); Data are presented as mean ± SD. (n=10). *p<0.01, ****p<0.0001, ns, not significant, two-tailed unpaired t test. (d), H&E staining of ISS and SOS sections showing loss of columnar organization of

Article Snippet: After blocking, the sections were incubated at 4 °C overnight, with the following primary antibodies: anti- DDR2 (LS B15752, 1:200), anti- Y740- P- DDR2 (R&D Systems MAB25382, 1:200), anti- cleaved caspase 3 (Cell Signaling 9661, 1:200), anti- COL2 (Abcam ab34712, 1:100); anti- COL10 (Abcam ab58632, 1:100); Anti- COL1(Millipore Sigma AB765P, 1:100); Anti- GM130 (BD Biosciences 610822,1:100); anti- IBSP (1:100).

Techniques: Knock-Out, Staining, Two Tailed Test

Journal: eLife

Article Title: Control of craniofacial development by the collagen receptor, discoidin domain receptor 2

doi: 10.7554/elife.77257

Figure Lengend Snippet: Figure 3. ECM defects in Ddr2-deficient synchondroses. (a-d) Immunofluorescent staining of ISS and SOS sections from 2-week-old WT and Ddr2slie/

Article Snippet: After blocking, the sections were incubated at 4 °C overnight, with the following primary antibodies: anti- DDR2 (LS B15752, 1:200), anti- Y740- P- DDR2 (R&D Systems MAB25382, 1:200), anti- cleaved caspase 3 (Cell Signaling 9661, 1:200), anti- COL2 (Abcam ab34712, 1:100); anti- COL10 (Abcam ab58632, 1:100); Anti- COL1(Millipore Sigma AB765P, 1:100); Anti- GM130 (BD Biosciences 610822,1:100); anti- IBSP (1:100).

Techniques: Staining

Journal: eLife

Article Title: Control of craniofacial development by the collagen receptor, discoidin domain receptor 2

doi: 10.7554/elife.77257

Figure Lengend Snippet: Figure 4. Ddr2 expression in craniofacial skeleton. (a) Whole-mount X-gal staining (green) of Ddr2Lacz/+ skulls showing of Ddr2 expression in midfacial region, cranial vault, and cranial sutures. Scale bar: 50 μm. (b) X-gal staining of cryostat sections of calvaria from newborn mice showing expression in suture mesenchyme, periosteum, and dura mater of flanking bones. Scale bar: 100 μm, left and 50 μm, right. (c) X-gal staining of cryostat section of ISS (top) and SOS (bottom) from newborn mice revealing Ddr2 expression in resting and proliferative chondrocyte zones, but low or undetected in terminal hypertrophic chondrocytes. Boxed regions are shown in higher magnification, right. Scale bar: 50 μm.

Article Snippet: After blocking, the sections were incubated at 4 °C overnight, with the following primary antibodies: anti- DDR2 (LS B15752, 1:200), anti- Y740- P- DDR2 (R&D Systems MAB25382, 1:200), anti- cleaved caspase 3 (Cell Signaling 9661, 1:200), anti- COL2 (Abcam ab34712, 1:100); anti- COL10 (Abcam ab58632, 1:100); Anti- COL1(Millipore Sigma AB765P, 1:100); Anti- GM130 (BD Biosciences 610822,1:100); anti- IBSP (1:100).

Techniques: Expressing, Staining

Journal: eLife

Article Title: Control of craniofacial development by the collagen receptor, discoidin domain receptor 2

doi: 10.7554/elife.77257

Figure Lengend Snippet: Figure 6. Loss of Ddr2 in Gli1-expressing cells resulted in a craniofacial phenotype similar to Ddr2slie/slie mice. (a) Protocol used for induction of Cre- recombination upon tamoxifen injection. (b) Genotyping PCR showing WT (lower band) and Ddr2 floxed alleles (upper band) near 1650 bp and recombined knockout allele below the 650 bp marker (KO). (c) Top head view showing Gli1CreERT; Ddr2fl/fl mice have short snout compared with Ddr2fl/fl mice. Scale bar: 1 cm. (d) μCT scans of Ddr2fl/fl and Gli1CreERT; Ddr2fl/fl skulls show reduced anterior-posterior skull length and increased anterior skull width (quantification in e–g). Note thinning and suture defect in the frontal bone in Gli1CreERT; Ddr2fl/fl skulls (d, bottom). Scale bar: 1 mm. (h) Quantification of frontal, parietal, and occipital bone thickness. (i) Alcian blue and Alizarin red whole mount staining shows Gli1-Cre; Ddr2fl/fl skulls have wide cranial base synchondroses compared with Gli1CreERT and Ddr2fl/fl. Scale bar: 500 μm. (j) H&E staining of ISS shows widening of resting zone and chondrocyte disorganization in Gli1CreERT; Ddr2fl/fl mice. Scale bar: 50 μm. RZ: Resting zone; PZ: Proliferative zone; HZ: Hypertrophic zone. Red bar compares RZ width. (k) Immunofluorescence images show reduced pDDR2 (red) immunostaining indicative of reduced DDR2 signaling in Gli1CreERT; Ddr2fl/fl synchondrosis. Dotted lines denote chondro-osseous junction. Boxed region is shown in higher magnification, lower panel. Cell nuclei were stained with DAPI (blue). Arrows, resting zone; arrowheads, proliferative zone. Scale bar: 50 μm. (l), quantification of immunostaining in k. (m-p) μCT images and quantification show enlarged synchondroses associated with shortening in cranial base bone lengths in 3-month-old Gli1CreERT; Ddr2fl/fl skulls compared with controls. Scale bar: 500 μm. c-h, (m-p) 3-month-old mice. (i–l) 2-week-old mice. Data are presented as mean ± SD. (n=10). *p<0.01, **p<0.01, ***p<0.001, ****p<0.0001, ns, not significant, two-tailed unpaired t test.

Article Snippet: After blocking, the sections were incubated at 4 °C overnight, with the following primary antibodies: anti- DDR2 (LS B15752, 1:200), anti- Y740- P- DDR2 (R&D Systems MAB25382, 1:200), anti- cleaved caspase 3 (Cell Signaling 9661, 1:200), anti- COL2 (Abcam ab34712, 1:100); anti- COL10 (Abcam ab58632, 1:100); Anti- COL1(Millipore Sigma AB765P, 1:100); Anti- GM130 (BD Biosciences 610822,1:100); anti- IBSP (1:100).

Techniques: Expressing, Injection, Knock-Out, Marker, Staining, Immunofluorescence, Immunostaining, Two Tailed Test

Journal: eLife

Article Title: Control of craniofacial development by the collagen receptor, discoidin domain receptor 2

doi: 10.7554/elife.77257

Figure Lengend Snippet: Figure 7. Ddr2 conditional knockout in Col2a1-expressing chondrocytes causes cranial base hypoplasia and alters synchondroses without affecting cranial sutures. (a-d) μCT scans of Ddr2fl/fl and Col2a1Cre;Ddr2fl/fl skulls (3-month-old) showing reduced anterior-posterior skull length, length of individual bones and increased anterior and, to a lesser extent, posterior skull width in conditional knockout mice. Note thinning of frontal bone in Col2a1Cre;Ddr2fl/

Article Snippet: After blocking, the sections were incubated at 4 °C overnight, with the following primary antibodies: anti- DDR2 (LS B15752, 1:200), anti- Y740- P- DDR2 (R&D Systems MAB25382, 1:200), anti- cleaved caspase 3 (Cell Signaling 9661, 1:200), anti- COL2 (Abcam ab34712, 1:100); anti- COL10 (Abcam ab58632, 1:100); Anti- COL1(Millipore Sigma AB765P, 1:100); Anti- GM130 (BD Biosciences 610822,1:100); anti- IBSP (1:100).

Techniques: Knock-Out, Expressing

Journal: Breast cancer research : BCR

Article Title: Parity predisposes breasts to the oncogenic action of PAPP-A and activation of the collagen receptor DDR2.

doi: 10.1186/s13058-019-1142-z

Figure Lengend Snippet: Fig. 3 PAPP-A promotes DDR2 activation through collagen mRNA stabilization and IGF signaling in vitro. a Schematic of the proposed mechanism of activation of DDR2/Snail signaling axis of invasion [39]. b Representative images of Snail IHC (Snail: red; nuclei: blue) of virgin, involuting, or post- partum mammary glands from non-transgenic or PAPP-A transgenic mice. n = 5 mice per group. Quantification of Snail IHC is shown, n = 5 mice per group. Mean ± SEM, unpaired t test with Welch’s correction (comparisons between the score 3 group only). *p < 0.05, **p < 0.005. c Immunoblot of indicated markers in MCF-7 or MCF-7PAPP-A cells co-cultured with and without collagen. Scale bar 100 μm. d Representative images of 48 h Transwell in vitro invasion assays of MCF-7 and MCF-7PAPP-A cells. Experiments repeated in technical triplicate. Scale bar 100 μm. Quantification is shown, unpaired t test with Welch’s correction. *p < 0.05. e Relative fold change of col1a1 mRNA transcript in MCF-7PAPP-A over MCF-7 cells measured by real-time qPCR and normalized to actin. Mean + SEM, triplicate experiment. Unpaired t test with Welch’s correction. *p < 0.05. f Relative fold change of col1a1 mRNA transcript in MCF-7 cells treated in vitro with or without PAPP-A media for 24 h. PAPP-A media concentration is at 10 ng/mL of PAPP-A protein (quantified by ELISA). Measured by real-time qPCR and normalized to actin. Mean + SEM, triplicate experiment. Unpaired t test with Welch’s correction. **p < 0.005. g Immunoblot of LARP6 in MCF-7 cells treated in vitro with or without PAPP-A media for 24 h. PAPP-A media concentration is at 10 ng/mL of PAPP-A protein (quantified by ELISA). h Representative immunoblot of LARP6 in the mammary glands from non-transgenic or PAPP-A transgenic mice during virgin, involution, or late post-partum. n = 5 mice per group. i Immunoblot of rIGFBP-5 following a 3-h incubation in culture media from MCF-7 (CTL), MCF-7PAPP-A (PA), or MCF-7 overexpressing proteolytic-dead mutant PAPP-A E483Q (E483Q). Immunoblot of PAPP-A secreted in culture media from MCF-7, MCF-7PAPP-A, and MCF-7PAPP-A/E483Q cells. j Immunoblot of MCF-7 cells treated in vitro with culture media from MCF-7 (CTL), MCF- 7PAPP-A (PA), or MCF-7PAPP-A/E483Q (E483Q) cells for 24 h. k Immunoblot of DDR2 and phospho-DDR2 in MCF-7 and MCF-7PAPP-A cells treated in vitro with recombinant IGF-1 at 10 nM for indicated time points

Article Snippet: Thirty micrograms total protein in 1× Laemmli buffer per sample was separated on a 10% SDS-glycine polyacrylamide gels ran at 80 V for 30 min and 200 V for 45 min. Proteins were transferred to nitrocellulose membranes (GE Healthcare) for 1.5 h at 85 V. Membranes were blocked in 5% milk in TBS-T and incubated on a rotator overnight at 4 °C in the following primary antibodies: DDR2 1:250 (Cell Signaling Technology #12133S), p-DDR2 Y740 1:600 (R&D Systems, #MAB25382), Snail 1:1000 (Cell Signaling Technology L70G2 #3895), Larp6 1:600 (Abnova, #H00055323-B01P), IGFBP-5 1:1000 (EMD Millipore, #06-110), PAPP-A 1:200 (Santa Cruz Biotechnology, # sc-50518), phospho-Akt (Ser473) 1:1000 (Cell Signaling Technology 587F11 #4051), Akt 1:10,000 (Cell Signaling Technology #9272), and actin 1:10,000 (EMB Millipore #MAB1501R).

Techniques: Activation Assay, In Vitro, Transgenic Assay, Western Blot, Cell Culture, Concentration Assay, Enzyme-linked Immunosorbent Assay, Incubation, Mutagenesis, Recombinant

Journal: Breast cancer research : BCR

Article Title: Parity predisposes breasts to the oncogenic action of PAPP-A and activation of the collagen receptor DDR2.

doi: 10.1186/s13058-019-1142-z

Figure Lengend Snippet: Fig. 4 Loss of DDR2 abolishes cell invasion, Snail expression, and tumor growth by PAPP-A. a Immunoblot of indicated markers in MCF-7PAPP-A

Article Snippet: Thirty micrograms total protein in 1× Laemmli buffer per sample was separated on a 10% SDS-glycine polyacrylamide gels ran at 80 V for 30 min and 200 V for 45 min. Proteins were transferred to nitrocellulose membranes (GE Healthcare) for 1.5 h at 85 V. Membranes were blocked in 5% milk in TBS-T and incubated on a rotator overnight at 4 °C in the following primary antibodies: DDR2 1:250 (Cell Signaling Technology #12133S), p-DDR2 Y740 1:600 (R&D Systems, #MAB25382), Snail 1:1000 (Cell Signaling Technology L70G2 #3895), Larp6 1:600 (Abnova, #H00055323-B01P), IGFBP-5 1:1000 (EMD Millipore, #06-110), PAPP-A 1:200 (Santa Cruz Biotechnology, # sc-50518), phospho-Akt (Ser473) 1:1000 (Cell Signaling Technology 587F11 #4051), Akt 1:10,000 (Cell Signaling Technology #9272), and actin 1:10,000 (EMB Millipore #MAB1501R).

Techniques: Expressing, Western Blot

Journal: Breast cancer research : BCR

Article Title: Parity predisposes breasts to the oncogenic action of PAPP-A and activation of the collagen receptor DDR2.

doi: 10.1186/s13058-019-1142-z

Figure Lengend Snippet: Fig. 6 PAPP-A/SNAI1/COL1A1 gene signature correlates with distant metastasis in breast cancer patients. a Heatmap of patients clustered based on their score for the PAPP-A/SNAI1/COL1A1 signature (categorized according to the mean score value). Each row represents one patient, n = 327. b Kaplan-Meier curve for time to distant metastasis according to the PAPP-A/SNAI1/COL1A1 score as defined in a. Number of patients at risk at each time point over a 150-month period is recorded below in table. c Heatmap representing the relative expression of a selected panel of 78 genes (FDR < .05) in the PAPP-A/SNAI1/COL1A1-low and PAPP-A/SNAI1/COL1A1-high patient populations. Genes are organized by pathways, as labeled adjacent to the gene names. The red text highlights relevant genes investigated in this study (PAPP-A, DDR2, SNAI1, COL1A1, and LARP6). Each column represents a patient, and each row represents a gene. d Chart of GSEA pathways significantly enriched in the PAPP-A/SNAI1/COL1A1-high patient population. Each bar represents the normalized enrichment score of the indicated pathway

Article Snippet: Thirty micrograms total protein in 1× Laemmli buffer per sample was separated on a 10% SDS-glycine polyacrylamide gels ran at 80 V for 30 min and 200 V for 45 min. Proteins were transferred to nitrocellulose membranes (GE Healthcare) for 1.5 h at 85 V. Membranes were blocked in 5% milk in TBS-T and incubated on a rotator overnight at 4 °C in the following primary antibodies: DDR2 1:250 (Cell Signaling Technology #12133S), p-DDR2 Y740 1:600 (R&D Systems, #MAB25382), Snail 1:1000 (Cell Signaling Technology L70G2 #3895), Larp6 1:600 (Abnova, #H00055323-B01P), IGFBP-5 1:1000 (EMD Millipore, #06-110), PAPP-A 1:200 (Santa Cruz Biotechnology, # sc-50518), phospho-Akt (Ser473) 1:1000 (Cell Signaling Technology 587F11 #4051), Akt 1:10,000 (Cell Signaling Technology #9272), and actin 1:10,000 (EMB Millipore #MAB1501R).

Techniques: Expressing, Labeling

Journal: Breast cancer research : BCR

Article Title: Parity predisposes breasts to the oncogenic action of PAPP-A and activation of the collagen receptor DDR2.

doi: 10.1186/s13058-019-1142-z

Figure Lengend Snippet: Fig. 7 Model of PAPP-A-driven PABC. Schematic of our current understanding of PAPP-A-driven PABC, where red boxes indicate factors that have been established to activate the pathway, blue boxes indicate factors inhibiting the pathway, and green boxes factors that are hypothesized to affect the pathway. In this model, elevated content in collagen is necessary for PAPP-A to cleave IGFBP-5 in the mammary gland. The elevated level of collagen can be provided through distinct avenues including involution and, as demonstrated in the current study, post-partum environment. We postulate that high breast density may contribute the activity of PAPP-A. Conversely, extended breastfeeding appears to inhibit PAPP-A. Upon activation of PAPP-A and cleavage of IGFBP-5, free IGFs are released and able to bind and activate the IGF receptor, which results in increased IGF signaling, increased collagen deposition, and extended involution, in the case of an involuting mammary gland. We show that LARP6 is activated following PAPP-A overexpression and as a chaperone of the mRNA of collagen, LARP6 contributes to the elevation in collagen deposition in PAPP-A-driven mammary tumors. In addition, the collagen receptor DDR2 is activated, which leads to the DDR2/Snail axis of metastasis reported by others. In a mechanism that remains unclear, DDR2 promotes the formation of TACS3 collagen, which facilitates metastasis

Article Snippet: Thirty micrograms total protein in 1× Laemmli buffer per sample was separated on a 10% SDS-glycine polyacrylamide gels ran at 80 V for 30 min and 200 V for 45 min. Proteins were transferred to nitrocellulose membranes (GE Healthcare) for 1.5 h at 85 V. Membranes were blocked in 5% milk in TBS-T and incubated on a rotator overnight at 4 °C in the following primary antibodies: DDR2 1:250 (Cell Signaling Technology #12133S), p-DDR2 Y740 1:600 (R&D Systems, #MAB25382), Snail 1:1000 (Cell Signaling Technology L70G2 #3895), Larp6 1:600 (Abnova, #H00055323-B01P), IGFBP-5 1:1000 (EMD Millipore, #06-110), PAPP-A 1:200 (Santa Cruz Biotechnology, # sc-50518), phospho-Akt (Ser473) 1:1000 (Cell Signaling Technology 587F11 #4051), Akt 1:10,000 (Cell Signaling Technology #9272), and actin 1:10,000 (EMB Millipore #MAB1501R).

Techniques: Activity Assay, Activation Assay, Over Expression