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mouse anti fgfr1 (R&D Systems)

Name: mouse anti fgfr1
Brand: R&D Systems
Rating: 93 (22 reviews)

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R&D Systems mouse anti fgfr1
Secreted proteins significantly changed in both RNA and protein abundances in both Rebl.PAT and Man-13 cell lines.

Mouse Anti Fgfr1, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 22 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/mouse anti fgfr1/product/R&D Systems
Average 93 stars, based on 22 article reviews

mouse anti fgfr1 - by Bioz Stars, 2026-03

93/100 stars

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1) Product Images from "A secreted proteomic footprint for stem cell pluripotency"

Article Title: A secreted proteomic footprint for stem cell pluripotency

Journal: PLOS ONE

doi: 10.1371/journal.pone.0299365

Figure Legend Snippet: Secreted proteins significantly changed in both RNA and protein abundances in both Rebl.PAT and Man-13 cell lines.

Techniques Used:

Equal quantities of protein from media supernatant from cells cultured as described in were run on Western blot and probed with antibodies for an E8-enriched marker protein (CHGA, NID1, SEMA3 or NPTX3) and an E6-enriched marker protein (COCH, FGFR1, Follistatin or OLFML3). Membranes were imaged using LICOR Odyssey system.

Figure Legend Snippet: Equal quantities of protein from media supernatant from cells cultured as described in were run on Western blot and probed with antibodies for an E8-enriched marker protein (CHGA, NID1, SEMA3 or NPTX3) and an E6-enriched marker protein (COCH, FGFR1, Follistatin or OLFML3). Membranes were imaged using LICOR Odyssey system.

Techniques Used: Cell Culture, Western Blot, Marker

Image Search Results

Figure 3. ECM1 activates the MAPK signaling pathway in PCa cells. A) Waterfall plot showing diﬀerentially expressed genes (p < 0.05, log2 fold change>1.5) in C4-2B cells treated with ENZ (10 μM, 48 h) combined with ECM1 protein (200 ng mL−1, 48 h) or ENZ (10 μM, 48 h) alone. The highlighted genes were related to proliferation and apoptosis. B) KEGG analysis of pathways enriched in ENZ combined with ECM1 protein treatment group compared to the ENZ treatment group. C) WB analysis of MEK, p-MEK, ERK1/2, and p-ERK1/2 expression in the indicated groups of C4-2B cells. D) IHC staining and quantiﬁcation of p-ERK1/2 expression in mice intratibial and subcutaneous tumors grouped as indicated (Scale bars, 500 μm and 100 μm, n = 6 per group). E) WB analysis and quantiﬁcation of MEK, p-MEK, ERK1/2, and p-ERK1/2 expression in C4-2B cells stimulated with ENZ (10 μM) combined with ECM1 (200 ng mL−1) in the presence of inhibitors for either RAS (MCP110, 10 μM), MEK (U0126, 10 μM), ERK1/2 (Ulixertinib, 10 μM), EGFR (Lapatinib, 10 μM), FGFR1 (Fexagratinib, 10 μM), IGF1R (Linsitinib, 10 μM) or Veh (DMSO), compared to ENZ-treated alone or untreated C4-2B cells. F) C4-2B cell proliferation on day 7 of groups as shown in E. G) WB analysis and quantiﬁcation of EGFR, p-EGFR, FGFR1, p-FGFR1, IGF1R and p-IGF1R expression in groups as indicated. ns, not signiﬁcant; *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.

Journal: Advanced science (Weinheim, Baden-Wurttemberg, Germany)

Article Title: Osteoblast-Derived ECM1 Promotes Anti-Androgen Resistance in Bone Metastatic Prostate Cancer.

doi: 10.1002/advs.202407662

Figure Lengend Snippet: Figure 3. ECM1 activates the MAPK signaling pathway in PCa cells. A) Waterfall plot showing diﬀerentially expressed genes (p < 0.05, log2 fold change>1.5) in C4-2B cells treated with ENZ (10 μM, 48 h) combined with ECM1 protein (200 ng mL−1, 48 h) or ENZ (10 μM, 48 h) alone. The highlighted genes were related to proliferation and apoptosis. B) KEGG analysis of pathways enriched in ENZ combined with ECM1 protein treatment group compared to the ENZ treatment group. C) WB analysis of MEK, p-MEK, ERK1/2, and p-ERK1/2 expression in the indicated groups of C4-2B cells. D) IHC staining and quantiﬁcation of p-ERK1/2 expression in mice intratibial and subcutaneous tumors grouped as indicated (Scale bars, 500 μm and 100 μm, n = 6 per group). E) WB analysis and quantiﬁcation of MEK, p-MEK, ERK1/2, and p-ERK1/2 expression in C4-2B cells stimulated with ENZ (10 μM) combined with ECM1 (200 ng mL−1) in the presence of inhibitors for either RAS (MCP110, 10 μM), MEK (U0126, 10 μM), ERK1/2 (Ulixertinib, 10 μM), EGFR (Lapatinib, 10 μM), FGFR1 (Fexagratinib, 10 μM), IGF1R (Linsitinib, 10 μM) or Veh (DMSO), compared to ENZ-treated alone or untreated C4-2B cells. F) C4-2B cell proliferation on day 7 of groups as shown in E. G) WB analysis and quantiﬁcation of EGFR, p-EGFR, FGFR1, p-FGFR1, IGF1R and p-IGF1R expression in groups as indicated. ns, not signiﬁcant; *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001.

Article Snippet: GAPDH was used as the loading control. ns, not significant; *, P < 0.05; **, P < 0.01; ***, P < 0.001; ****, P < 0.0001. nology; #4695, 1:1000), Phospho-ERK1/2 (Thr202/Tyr204) Rabbit mAb (Cell Signaling Technology; #4370, 1:2000), EGFR Rabbit mAb (Cell Signaling Technology; #4267, 1:1000), Phospho-EGFR (Tyr978) Rabbit mAb (Cell Signaling Technology; #3790, 1:1000), IGF1R Rabbit mAb (Cell Signaling Technology; #9750, 1:1000), Phospho-IGF1R Rabbit mAb (Cell Signaling Technology; #3918, 1:1000), FGFR1 Mouse mAb (Proteintech; 60325-1-Ig, 1:1000), Phospho-FGFR1 (Tyr653/Tyr654) Rabbit pAb (Sigma Aldrich; 06– 1433, 1:1000) and Phospho-Tyrosine Mouse mAb (P-Tyr-100) (Cell Signaling Technology; #9411, 1:2000).

Techniques: Expressing, Immunohistochemistry

Journal: PLOS ONE

Article Title: A secreted proteomic footprint for stem cell pluripotency

doi: 10.1371/journal.pone.0299365

Figure Lengend Snippet: Secreted proteins significantly changed in both RNA and protein abundances in both Rebl.PAT and Man-13 cell lines.

Article Snippet: Gels were transferred using the IBlot2 Gel Transfer device (Thermo #IB21001), using iBlot 2 Transfer stacks (nitrocellulose membrane, Thermo #IB23001).Cells were analysed by immunoblotting using the following antibodies: 1/200 Mouse anti-Chromogranin A (Novus Biologicalis, NBP2-44774); 1/100 Rabbit anti-COCH (Abcam, ab170266); 1/500 mouse anti-FGFR1 (R&D systems, MAB658); 1/1000 rabbit anti-Follistatin (Abcam, ab157471); 1/1000 rabbit anti-Entactin/NID1 (Abcam, ab133686); 1:1000 rabbit anti-Neuronal Pentaxtrin 2 (Abcam, ab191563); 1/1000 rabbit anti-Neurotensin (Abcam, ab172114); 1/300 rabbit anti-Olfactomedin-like 3 (Abcam, ab111712); 1/500 mouse anti-Semaphorin 3A (R&D, MAB1250); 1/500 mouse anti-Secreted Frizzled Related Protein 2 (R&D, MAB6838).

Techniques:

Journal: PLOS ONE

Article Title: A secreted proteomic footprint for stem cell pluripotency

doi: 10.1371/journal.pone.0299365

Figure Lengend Snippet: Equal quantities of protein from media supernatant from cells cultured as described in were run on Western blot and probed with antibodies for an E8-enriched marker protein (CHGA, NID1, SEMA3 or NPTX3) and an E6-enriched marker protein (COCH, FGFR1, Follistatin or OLFML3). Membranes were imaged using LICOR Odyssey system.

Techniques: Cell Culture, Western Blot, Marker

FGF signalling is required for timely PNP closure. (A) Whole-mount stained confocal images showing pERK1/2 immunolocalization in vehicle- and pan-FGFRi-treated embryos after 24 h of whole-embryo culture. pERK-bright cells persist around the PNP rim in the pan-FGFRi-treated embryo. Scale bar: 100 µm. (B) Whole-mount Fgf8 in situ hybridisation in vehicle- and pan-FGFRi-treated embryos after 8 h of whole-embryo culture. Dashed white lines indicate the end of the tailbud; arrows indicate the forelimb buds. Scale bar: 500 µm. (C) Bright-field images showing RARE-mediated LacZ expression domain in vehicle and pan-FGFRi-treated embryos after 24 h of whole-embryo culture. An equivalently processed negative (−ve) control embryo lacking LacZ is also shown. The white bracket indicates the distance between the RARE domain and the zippering point. The black bracket indicates that the RARE domain does not extend to the end of the PNP in pan-FGFRi-treated embryos. Scale bar: 350 µm. (D) Quantification of RARE domain distance to the end of zippering point in vehicle and pan-FGFRi-treated embryos after 24 h of whole-embryo culture. Individual points represent data from individual embryos; P -value was calculated using an unpaired t -test. (E) Whole-mount immunolocalization of Fgfr1 in a 28-somite stage embryo. Scale bar: 100 µm. (F) Confocal images of embryos treated with vehicle or a second Fgfr1-targeting antagonist after 24 h of whole-embryo culture. Dashed red lines outline the abnormal neuroepithelium in inhibitor-treated embryos. Scale bar: 100 µm. (G) Quantification of the proportion of embryos with closed PNPs, open PNPs with Closure 5 morphology (caudally narrowed PNP with elevated caudal neural folds that meet dorsally) or open PNPs without Closure 5 in vehicle and FGFR1-targeting inhibitor-treated embryos after 24 h of whole-embryo culture. Numbers indicate the number of embryos observed in each category. Magenta asterisks indicate the rostral zippering point; cyan asterisks indicate Closure 5.

Journal: Development (Cambridge, England)

Article Title: Caudal Fgfr1 disruption produces localised spinal mis-patterning and a terminal myelocystocele-like phenotype in mice

doi: 10.1242/dev.202139

Figure Lengend Snippet: FGF signalling is required for timely PNP closure. (A) Whole-mount stained confocal images showing pERK1/2 immunolocalization in vehicle- and pan-FGFRi-treated embryos after 24 h of whole-embryo culture. pERK-bright cells persist around the PNP rim in the pan-FGFRi-treated embryo. Scale bar: 100 µm. (B) Whole-mount Fgf8 in situ hybridisation in vehicle- and pan-FGFRi-treated embryos after 8 h of whole-embryo culture. Dashed white lines indicate the end of the tailbud; arrows indicate the forelimb buds. Scale bar: 500 µm. (C) Bright-field images showing RARE-mediated LacZ expression domain in vehicle and pan-FGFRi-treated embryos after 24 h of whole-embryo culture. An equivalently processed negative (−ve) control embryo lacking LacZ is also shown. The white bracket indicates the distance between the RARE domain and the zippering point. The black bracket indicates that the RARE domain does not extend to the end of the PNP in pan-FGFRi-treated embryos. Scale bar: 350 µm. (D) Quantification of RARE domain distance to the end of zippering point in vehicle and pan-FGFRi-treated embryos after 24 h of whole-embryo culture. Individual points represent data from individual embryos; P -value was calculated using an unpaired t -test. (E) Whole-mount immunolocalization of Fgfr1 in a 28-somite stage embryo. Scale bar: 100 µm. (F) Confocal images of embryos treated with vehicle or a second Fgfr1-targeting antagonist after 24 h of whole-embryo culture. Dashed red lines outline the abnormal neuroepithelium in inhibitor-treated embryos. Scale bar: 100 µm. (G) Quantification of the proportion of embryos with closed PNPs, open PNPs with Closure 5 morphology (caudally narrowed PNP with elevated caudal neural folds that meet dorsally) or open PNPs without Closure 5 in vehicle and FGFR1-targeting inhibitor-treated embryos after 24 h of whole-embryo culture. Numbers indicate the number of embryos observed in each category. Magenta asterisks indicate the rostral zippering point; cyan asterisks indicate Closure 5.

Article Snippet: Primary antibodies were used at 1:100 dilution and were as follows: rabbit E-cadherin (3195, Cell Signaling Technology), mouse N-cadherin (14215S, Cell Signaling Technology), rabbit pERK1/2 (9101, Cell Signalling Technology), mouse FGFR1 (ab824, Abcam) mouse anti-RALDH2 (sc-166362, Santa Cruz) and rabbit anti pFGFR1 (Tyr 653/654, GTX133526, Stratech).

Techniques: Staining, Embryo Culture, In Situ, Hybridization, Expressing

Caudal genetic deletion of Fgfr1 impairs Closure 5 formation and the progression of PNP closure without diminishing embryo viability. (A) E10.5 embryos showing the Cdx2 Cre -recombination domain lineage traced using mTmG (EGFP) as a confocal-imaged cross-section and bright-field images. NT, neural tube; Som somite; SE, surface ectoderm. 1 and 2 indicate the forelimb (FL) to hindlimb (HL) and hindlimb to tail end distances, respectively, quantified in B. Scale bars: 100 µm (confocal); 400 µm (bright field). (B) Quantifications of FL-HL and HL-tail end lengths in 28-31 somite stage embryos. (C) Confocal images of whole-mount immunofluorescently stained embryos showing E- and N-cadherin localization in E10.5 embryos with no Cre and Cre;Fl/Fl littermate. Scale bar: 100 µm. (D) Whole-mount images of three phalloidin-stained Cre;Fl/Fl embryos collected at E10.5, suggesting continued PNP closure. Scale bar: 100 µm. (E) Quantification of PNP length versus somite stage in embryos collected at E9.5-E10.5. (F) Quantification of caudal neural fold elevation (90% of PNP length) in embryos collected at E9.5-E10.5. (G) Quantification of the proportion of embryos collected at E10.5 with closed PNPs, open PNPs with Closure 5 morphology or open PNPs without Closure 5. Numbers indicate the number of embryos observed in each category. Magenta asterisks indicate the rostral zippering point. P -value calculated using Fisher's exact test.

Journal: Development (Cambridge, England)

Article Title: Caudal Fgfr1 disruption produces localised spinal mis-patterning and a terminal myelocystocele-like phenotype in mice

doi: 10.1242/dev.202139

Figure Lengend Snippet: Caudal genetic deletion of Fgfr1 impairs Closure 5 formation and the progression of PNP closure without diminishing embryo viability. (A) E10.5 embryos showing the Cdx2 Cre -recombination domain lineage traced using mTmG (EGFP) as a confocal-imaged cross-section and bright-field images. NT, neural tube; Som somite; SE, surface ectoderm. 1 and 2 indicate the forelimb (FL) to hindlimb (HL) and hindlimb to tail end distances, respectively, quantified in B. Scale bars: 100 µm (confocal); 400 µm (bright field). (B) Quantifications of FL-HL and HL-tail end lengths in 28-31 somite stage embryos. (C) Confocal images of whole-mount immunofluorescently stained embryos showing E- and N-cadherin localization in E10.5 embryos with no Cre and Cre;Fl/Fl littermate. Scale bar: 100 µm. (D) Whole-mount images of three phalloidin-stained Cre;Fl/Fl embryos collected at E10.5, suggesting continued PNP closure. Scale bar: 100 µm. (E) Quantification of PNP length versus somite stage in embryos collected at E9.5-E10.5. (F) Quantification of caudal neural fold elevation (90% of PNP length) in embryos collected at E9.5-E10.5. (G) Quantification of the proportion of embryos collected at E10.5 with closed PNPs, open PNPs with Closure 5 morphology or open PNPs without Closure 5. Numbers indicate the number of embryos observed in each category. Magenta asterisks indicate the rostral zippering point. P -value calculated using Fisher's exact test.

Techniques: Staining

Regional deletion of Fgfr1 causes delayed PNP closure and localized terminal dilation of the neural tube central canal. (A) Proportion of control and Cre;Fl/Fl embryos collected with open spinal neural tubes at the days indicated. * P <0.05 by Fisher's exact test. (B) Whole-mount maximum projections flanked by optical cross-sections through the caudal end of a control and Cre;Fl/Fl littermate showing the neural tube (NT) and adjacent somites (Som). Scale bar: 100 µm. (C) Bright-field images showing the Cdx2 Cre recombination domain (green, EGFP) at E12.5 in a Cre;Fl/+ control and Cre;Fl/Fl littermate. The dashed white line indicates the dorsal tail border. Black arrows in the enlargement outline the cystic neural tube lumen. Scale bars: 300 µm (whole embryo); 150 µm (enlargement). BF, bright field; HL, hindlimb. (D) Whole-mount phalloidin-stained embryos showing the continuous, narrow neural tube lumen (arrows) in the control and dilated lumen (dashed white line) in the Cre;Fl/Fl embryo. Solid lines indicate the positions of sections taken through the same Cre;Fl/Fl embryo. Scale bars: 1 mm (whole mount) and 250 µm (sections). (E) Bright-field images of a control and littermate Cre;Fl/Fl fetuses collected at E14.5. Black arrows indicate the extent of the spinal lesion in the Cre;Fl/Fl embryo; white dashed line indicates its sac-like dilation. Scale bar: 750 µm. (F) Haematoxylin and Eosin-stained sections through control and Cre;Fl/Fl littermates collected at E14.5. Dashed black lines indicate continuous skin covering, # indicates cystic dilation of the spinal cord lumen; blue circles indicate the ventral vertebral body in the control, which is absent in the Cre;F/Fl. Scale bars: 300 µm (low magnification); 100 µm (high magnification).

Journal: Development (Cambridge, England)

Article Title: Caudal Fgfr1 disruption produces localised spinal mis-patterning and a terminal myelocystocele-like phenotype in mice

doi: 10.1242/dev.202139

Figure Lengend Snippet: Regional deletion of Fgfr1 causes delayed PNP closure and localized terminal dilation of the neural tube central canal. (A) Proportion of control and Cre;Fl/Fl embryos collected with open spinal neural tubes at the days indicated. * P <0.05 by Fisher's exact test. (B) Whole-mount maximum projections flanked by optical cross-sections through the caudal end of a control and Cre;Fl/Fl littermate showing the neural tube (NT) and adjacent somites (Som). Scale bar: 100 µm. (C) Bright-field images showing the Cdx2 Cre recombination domain (green, EGFP) at E12.5 in a Cre;Fl/+ control and Cre;Fl/Fl littermate. The dashed white line indicates the dorsal tail border. Black arrows in the enlargement outline the cystic neural tube lumen. Scale bars: 300 µm (whole embryo); 150 µm (enlargement). BF, bright field; HL, hindlimb. (D) Whole-mount phalloidin-stained embryos showing the continuous, narrow neural tube lumen (arrows) in the control and dilated lumen (dashed white line) in the Cre;Fl/Fl embryo. Solid lines indicate the positions of sections taken through the same Cre;Fl/Fl embryo. Scale bars: 1 mm (whole mount) and 250 µm (sections). (E) Bright-field images of a control and littermate Cre;Fl/Fl fetuses collected at E14.5. Black arrows indicate the extent of the spinal lesion in the Cre;Fl/Fl embryo; white dashed line indicates its sac-like dilation. Scale bar: 750 µm. (F) Haematoxylin and Eosin-stained sections through control and Cre;Fl/Fl littermates collected at E14.5. Dashed black lines indicate continuous skin covering, # indicates cystic dilation of the spinal cord lumen; blue circles indicate the ventral vertebral body in the control, which is absent in the Cre;F/Fl. Scale bars: 300 µm (low magnification); 100 µm (high magnification).

Techniques: Staining

Neuroepithelial commitment to post-mitotic neurons is not diminished by loss of Fgfr1 . (A) Immunofluorescent localization of the neuroepithelial marker SOX2 and epidermal marker E-cadherin (arrowheads) through the distal spinal cord of a control and Cre;Fl/Fl fetus. Scale bars: 100 µm. (B,C) Progenitor (SOX2) and committed neuron (B, TUJ1; C, HUC/D) immunofluorescence of sections through the low-lumbar spinal cord of a control and Cre;Fl/Fl embryo collected at E11.5. There are ectopic clusters of SOX2-positive cells below the neural tube of the Cre;Fl/Fl embryo (white arrows, described below). Scale bar: 100 µm. (D) Whole-mount confocal images showing TUJ1 immunolocalization in the dorsal aspect of a control and littermate Cre;Fl/Fl embryo collected at E11.5 and imaged equivalently. Dashed white lines indicate the body outline. HL, hindlimb. Scale bar: 100 µm.

Journal: Development (Cambridge, England)

Article Title: Caudal Fgfr1 disruption produces localised spinal mis-patterning and a terminal myelocystocele-like phenotype in mice

doi: 10.1242/dev.202139

Figure Lengend Snippet: Neuroepithelial commitment to post-mitotic neurons is not diminished by loss of Fgfr1 . (A) Immunofluorescent localization of the neuroepithelial marker SOX2 and epidermal marker E-cadherin (arrowheads) through the distal spinal cord of a control and Cre;Fl/Fl fetus. Scale bars: 100 µm. (B,C) Progenitor (SOX2) and committed neuron (B, TUJ1; C, HUC/D) immunofluorescence of sections through the low-lumbar spinal cord of a control and Cre;Fl/Fl embryo collected at E11.5. There are ectopic clusters of SOX2-positive cells below the neural tube of the Cre;Fl/Fl embryo (white arrows, described below). Scale bar: 100 µm. (D) Whole-mount confocal images showing TUJ1 immunolocalization in the dorsal aspect of a control and littermate Cre;Fl/Fl embryo collected at E11.5 and imaged equivalently. Dashed white lines indicate the body outline. HL, hindlimb. Scale bar: 100 µm.

Techniques: Marker, Immunofluorescence

Localized progressive loss of ventral spinal progenitor domains precedes cystic dilation of the neural tube central canal in Fgfr1-disrupted embryos. (A) Immunofluorescent localization of the pMN marker OLIG2, floorplate marker SHH and neuron marker TUJ1 through the lumbar spinal cord of a control and Cre;Fl/Fl littermate collected at E11. White boxes indicate the regions shown at higher magnification; dashed white lines border the ventral neural tube; green polygon indicates the region ventral to the OLIG2 domain quantified in B; asterisks indicate the dorsal root ganglia; arrowhead indicates ectopic Shh-expressing tissue; arrow indicates TUJ1-positive projection from the ectopic tissue. Scale bars: 50 µm (higher magnification). (B) Quantification of the region of the neural tube ventral to the OLIG2 domain (‘floor plate’) as a proportion of neural tube area in control and Cre;Fl/Fl embryos collected at E10.5 and sectioned between the hindlimb buds. (C) Immunofluorescent localization of the intermediate neural progenitor marker PAX6 and dorsal/neural crest marker PAX3 in E11.5 embryos. PAX3 also labels cells in the neural crest-derived dorsal root ganglia (asterisk) and somite-derived dermomyotome (#). Dashed white lines outline the neural tube; dotted lines indicate the ventral extent of each domain. Serial sections in the Cre;Fl/Fl embryos are ∼50 µm apart. Scale bar: 50 µm.

Journal: Development (Cambridge, England)

Article Title: Caudal Fgfr1 disruption produces localised spinal mis-patterning and a terminal myelocystocele-like phenotype in mice

doi: 10.1242/dev.202139

Figure Lengend Snippet: Localized progressive loss of ventral spinal progenitor domains precedes cystic dilation of the neural tube central canal in Fgfr1-disrupted embryos. (A) Immunofluorescent localization of the pMN marker OLIG2, floorplate marker SHH and neuron marker TUJ1 through the lumbar spinal cord of a control and Cre;Fl/Fl littermate collected at E11. White boxes indicate the regions shown at higher magnification; dashed white lines border the ventral neural tube; green polygon indicates the region ventral to the OLIG2 domain quantified in B; asterisks indicate the dorsal root ganglia; arrowhead indicates ectopic Shh-expressing tissue; arrow indicates TUJ1-positive projection from the ectopic tissue. Scale bars: 50 µm (higher magnification). (B) Quantification of the region of the neural tube ventral to the OLIG2 domain (‘floor plate’) as a proportion of neural tube area in control and Cre;Fl/Fl embryos collected at E10.5 and sectioned between the hindlimb buds. (C) Immunofluorescent localization of the intermediate neural progenitor marker PAX6 and dorsal/neural crest marker PAX3 in E11.5 embryos. PAX3 also labels cells in the neural crest-derived dorsal root ganglia (asterisk) and somite-derived dermomyotome (#). Dashed white lines outline the neural tube; dotted lines indicate the ventral extent of each domain. Serial sections in the Cre;Fl/Fl embryos are ∼50 µm apart. Scale bar: 50 µm.

Techniques: Marker, Expressing, Derivative Assay

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1) Product Images from "A secreted proteomic footprint for stem cell pluripotency"

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