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Boster Bio primary antibodies against lif
Primary Antibodies Against Lif, supplied by Boster Bio, used in various techniques. Bioz Stars score: 90/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/primary+antibodies+against+lif/Anti-LIF+Reference+Antibody/pm36546418-74-0-17
Average 90 stars, based on 3 article reviews

primary antibodies against lif - by Bioz Stars, 2026-09

90/100 stars

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Journal: Nature Communications

Article Title: Cytoplasmic LIF reprograms invasive mode to enhance NPC dissemination through modulating YAP1-FAK/PXN signaling

doi: 10.1038/s41467-018-07660-6

Figure Lengend Snippet: Elevated cytoplasmic LIF and LIFR in NPC are correlated with poorer prognosis. a Representative images of LIF expression in adjacent normal epithelium and NPC tumor tissues. Scale bars, 20 μm. b Statistical analysis of cytoplasmic LIF expression in primary NPC tumor tissues and metastatic lesions. Analysis of cytoplasmic LIF expression in distinct metastatic lesions is shown (right). ** p < 0.01, *** p < 0.001, chi-square test. c Kaplan–Meier survival curves of NPC patients based on IHC scores of cytoplasmic LIF expression. Metastasis-free survival (left). Recurrence-free survival (right). d Statistical analysis of LIFR expression in NPC tumor biopsies. ** p < 0.01, chi-square test. e Kaplan–Meier survival analysis of NPC patients based on LIFR expression. Metastasis-free survival (left). Recurrence-free survival (right). f Analysis of correlation between cytoplasmic LIF and LIFR expression (Spearman’s correlation test). g Representative images of LIF and LIFR expression patterns in NPC tumor tissues. Scale bars, 50 μm. h Single nucleotide variations in NPC biopsy samples ( n = 157). Circles are colored with respect to the corresponding mutation types. i LIF and LIFR expression in tumors from NPC patient carrying LIF signal peptide mutation (G20L). Scale bars, 50 μm

Article Snippet: Blots were probed with specific primary antibodies against LIF (Abcam, ab135629, 1:500), LIFR (Santa Cruz Biotechnology, sc-515337, 1:500), phospho-YAP1 (Cell Signaling, 13008, 1:2000), YAP1 (Cell Signaling, 14074, 1:2000), phospho-FAK (Invitrogen, 700255, 1:5000), FAK (Santa Cruz Biotechnology, sc-558, 1:500), PECAM-1 (CD31) (Santa Cruz Biotechnology, sc-376764, 1:500), VE-cad (Santa Cruz Biotechnology, sc-9989, 1:1000), E-cad (BD Transduction Laboratories, 610181, 1:5000), phospho-PXN (Y118) (Abcam, ab109547, 1:4000), PXN (BD Transduction Laboratories, 610052, 1:10,000), phospho-p70S6K1 (T389) (Cell Signaling, 9234, 1:2000), p70S6K1 (Abcam, ab32529, 1:10,000), N-cad (Abcam, ab76011, 1:10,000), VIM (Sigma-Aldrich, V5255, 1:500), IQGAP1 (Santa Cruz Biotechnology, sc-81906, 1:1000), phospho-SRC (Cell Signaling, 6942, 1:2000), SRC (Cell Signaling, 2109, 1:2000), TKS5 (Proteintech, 18976-1-AP, 1:1500), CTTN (Abcam, ab81208, 1:10,000), MMP2 (Proteintech, 10373-2-AP, 1:800), and GAPDH (Abcam, ab8245, 1:5000) by incubation with horseradish peroxidase-conjugated secondary antibody and developed with enhanced chemiluminescence detection reagent (GE Healthcare).

Techniques: Expressing, Mutagenesis

Characterization of LIF mutant clones. a Sequence analysis of the LIF gene. Genomic DNA was extracted from parental NPC BM1 cells with wild-type LIF or established clones either with mutations in the signal peptide region of LIF (cLIF clone) or loss of the initiating codon in one allele (LIF +/− clone). The initiating codon within the spacer is indicated in red. Mutated nucleotides are marked in blue. b Assessment of LIF protein expression via western blot using GAPDH as a loading control. c Assessment of secreted LIF using a bead-based cytokine assay. Supernatants were harvested 2 days post culture. Data are presented as means ± SD of triplicate experiments. ** p < 0.01, two-tailed, paired t test. d Immunofluorescent detection of LIF (green) in WT, cLIF and LIF +/− cancer cells. Blue, nuclear staining. Scale bars, 10 μm. e Comparison of morphological changes (DIC images) in WT, cLIF, and LIF +/− cancer cells. Scale bars, 10 μm. f Live images of LIF uptake in cancer cells expressing LifeAct-RFP. Recombinant LIF proteins were pre-labeled with ATTO 488 green fluorescent dye. Images were captured 40 min post-LIF addition. g Time-course analysis of LIFR desensitization and p70S6K1 activation in LIF (30 ng/ml)-stimulated cells using GAPDH as a loading control

Journal: Nature Communications

Article Title: Cytoplasmic LIF reprograms invasive mode to enhance NPC dissemination through modulating YAP1-FAK/PXN signaling

doi: 10.1038/s41467-018-07660-6

Figure Lengend Snippet: Characterization of LIF mutant clones. a Sequence analysis of the LIF gene. Genomic DNA was extracted from parental NPC BM1 cells with wild-type LIF or established clones either with mutations in the signal peptide region of LIF (cLIF clone) or loss of the initiating codon in one allele (LIF +/− clone). The initiating codon within the spacer is indicated in red. Mutated nucleotides are marked in blue. b Assessment of LIF protein expression via western blot using GAPDH as a loading control. c Assessment of secreted LIF using a bead-based cytokine assay. Supernatants were harvested 2 days post culture. Data are presented as means ± SD of triplicate experiments. ** p < 0.01, two-tailed, paired t test. d Immunofluorescent detection of LIF (green) in WT, cLIF and LIF +/− cancer cells. Blue, nuclear staining. Scale bars, 10 μm. e Comparison of morphological changes (DIC images) in WT, cLIF, and LIF +/− cancer cells. Scale bars, 10 μm. f Live images of LIF uptake in cancer cells expressing LifeAct-RFP. Recombinant LIF proteins were pre-labeled with ATTO 488 green fluorescent dye. Images were captured 40 min post-LIF addition. g Time-course analysis of LIFR desensitization and p70S6K1 activation in LIF (30 ng/ml)-stimulated cells using GAPDH as a loading control

Techniques: Mutagenesis, Clone Assay, Sequencing, Expressing, Western Blot, Control, Cytokine Assay, Two Tailed Test, Staining, Comparison, Recombinant, Labeling, Activation Assay

High cytoplasmic LIF enhances cancer vascular invasion . a Real-time impedance analysis. HUVEC cells were grown on E-plates until confluence. Cancer cells were added on top of the HUVEC layer at the indicated times (black arrow). data are presented as means and SD of triplicate experiments. b Representative images of HUVEC layer replacement assay. Equal numbers of cancer cells were plated on top of the confluent HUVEC layer and co-cultivated for 24 h. Cells were labeled with antibodies against pan-cytokeratin (red) and VE-cadherin (green). Yellow closed polygons indicate damaged HUVEC areas. Scale bars, 20 μm. c Quantification of displaced areas in b . Data are presented with scatter dot plot (mean ± SEM). Each black dot represents one captured image. Invaded areas were calculated using CellSens imaging software (Olympus). *** p < 0.001, Mann–Whitney test. d Live-cell imaging of the HUVEC replacement assay. Cancer cells stably expressing LiveAct-RFP were plated onto confluent HUVEC cells expressing LiveAct-GFP2. Live interactions were continuously monitored for 30 hours (see also Supplementary movies - ). e Addition of cancer cells to the HUVEC layer breaks down endothelial junctions. An equal number of cancer cells was added on the top of HUVEC layer and co-cultivated for 24 h before fixation. Cells were labeled with antibodies against pan-cytokeratin (red) and CD31 (green, upper panels) or pan-cytokeratin and VE-cadherin (green, bottom panels). Scale bars, 10 μm. f Western blot of CD31 and VE-cadherin expression using GAPDH as a loading control. g Representative image of Tg (fli1a:EGFP)y1 zebrafish embryo carrying cancer cells expressing LifeAct-RFP on day 6 post-cancer cell injection. Tumor-like structures (red) that spread through the vasculature (green) were observed. h Representative images of disseminated tumor-like structures in zebrafish embryos injected with WT, LIF +/− , or cLIF cells. Asterisks indicate the dissemination sites of tumor-like structures. i Quantification of tumor-like structures shown in h . Areas of tumor dots were calculated using CellSens imaging software. The number of counts was determined 6 days after injection with cancer cells. Data are presented with scatter dot plot (mean ± SEM). Each black dot represents one fish embryo. * p < 0.05, ** p < 0.01, *** p < 0.001, Mann–Whitney test

Journal: Nature Communications

Article Title: Cytoplasmic LIF reprograms invasive mode to enhance NPC dissemination through modulating YAP1-FAK/PXN signaling

doi: 10.1038/s41467-018-07660-6

Figure Lengend Snippet: High cytoplasmic LIF enhances cancer vascular invasion . a Real-time impedance analysis. HUVEC cells were grown on E-plates until confluence. Cancer cells were added on top of the HUVEC layer at the indicated times (black arrow). data are presented as means and SD of triplicate experiments. b Representative images of HUVEC layer replacement assay. Equal numbers of cancer cells were plated on top of the confluent HUVEC layer and co-cultivated for 24 h. Cells were labeled with antibodies against pan-cytokeratin (red) and VE-cadherin (green). Yellow closed polygons indicate damaged HUVEC areas. Scale bars, 20 μm. c Quantification of displaced areas in b . Data are presented with scatter dot plot (mean ± SEM). Each black dot represents one captured image. Invaded areas were calculated using CellSens imaging software (Olympus). *** p < 0.001, Mann–Whitney test. d Live-cell imaging of the HUVEC replacement assay. Cancer cells stably expressing LiveAct-RFP were plated onto confluent HUVEC cells expressing LiveAct-GFP2. Live interactions were continuously monitored for 30 hours (see also Supplementary movies - ). e Addition of cancer cells to the HUVEC layer breaks down endothelial junctions. An equal number of cancer cells was added on the top of HUVEC layer and co-cultivated for 24 h before fixation. Cells were labeled with antibodies against pan-cytokeratin (red) and CD31 (green, upper panels) or pan-cytokeratin and VE-cadherin (green, bottom panels). Scale bars, 10 μm. f Western blot of CD31 and VE-cadherin expression using GAPDH as a loading control. g Representative image of Tg (fli1a:EGFP)y1 zebrafish embryo carrying cancer cells expressing LifeAct-RFP on day 6 post-cancer cell injection. Tumor-like structures (red) that spread through the vasculature (green) were observed. h Representative images of disseminated tumor-like structures in zebrafish embryos injected with WT, LIF +/− , or cLIF cells. Asterisks indicate the dissemination sites of tumor-like structures. i Quantification of tumor-like structures shown in h . Areas of tumor dots were calculated using CellSens imaging software. The number of counts was determined 6 days after injection with cancer cells. Data are presented with scatter dot plot (mean ± SEM). Each black dot represents one fish embryo. * p < 0.05, ** p < 0.01, *** p < 0.001, Mann–Whitney test

Techniques: Labeling, Imaging, Software, MANN-WHITNEY, Live Cell Imaging, Stable Transfection, Expressing, Western Blot, Control, Injection

LIF regulates focal adhesion molecules. a Detection of endogenous focal adhesion kinases in cancer cells via western blot using GAPDH as a loading control. b LIF regulates the spatial distribution of activated focal adhesion kinases. Cells were labeled with antibodies against phospho-PXN (Y118) or phospho-FAK (Y397). Alexa Fluor 488 phalloidin (green) was used to stain F-actin. Blue, nuclear staining. Scale bars, 10 μm. c Live imaging of focal adhesion during transendothelial invasion. Cancer cells expressing LifeAct-RFP were pre-labeled with Talin-GFP and plated onto the HUVEC layer. Images were captured 24 h post-plating. Blue, nuclei labeled with Hoechst33342. Scale bars, 20 μm. The white arrow indicates the damaged area caused by Talin-rich elongated protrusion. d Representative images of LIF, p-PXN (Y118), and p-FAK (Y397) expression in paraffin-embedded consecutive NPC tissue sections. Scale bars, 50 μm. e , f Correlation analyses based on IHC scores (Spearman’s correlation test). Correlations were evident between LIF and p-FAK (Y397) ( e ) and LIF and p-PXN (Y118) ( f )

Journal: Nature Communications

Article Title: Cytoplasmic LIF reprograms invasive mode to enhance NPC dissemination through modulating YAP1-FAK/PXN signaling

doi: 10.1038/s41467-018-07660-6

Figure Lengend Snippet: LIF regulates focal adhesion molecules. a Detection of endogenous focal adhesion kinases in cancer cells via western blot using GAPDH as a loading control. b LIF regulates the spatial distribution of activated focal adhesion kinases. Cells were labeled with antibodies against phospho-PXN (Y118) or phospho-FAK (Y397). Alexa Fluor 488 phalloidin (green) was used to stain F-actin. Blue, nuclear staining. Scale bars, 10 μm. c Live imaging of focal adhesion during transendothelial invasion. Cancer cells expressing LifeAct-RFP were pre-labeled with Talin-GFP and plated onto the HUVEC layer. Images were captured 24 h post-plating. Blue, nuclei labeled with Hoechst33342. Scale bars, 20 μm. The white arrow indicates the damaged area caused by Talin-rich elongated protrusion. d Representative images of LIF, p-PXN (Y118), and p-FAK (Y397) expression in paraffin-embedded consecutive NPC tissue sections. Scale bars, 50 μm. e , f Correlation analyses based on IHC scores (Spearman’s correlation test). Correlations were evident between LIF and p-FAK (Y397) ( e ) and LIF and p-PXN (Y118) ( f )

Techniques: Western Blot, Control, Labeling, Staining, Imaging, Expressing

LIFR–YAP1 signaling is critical for LIF-mediated invasion of NPC cells. a Endogenous protein expression of LIFR, p-YAP1(S127), and YAP1 in three cancer cell lines. b Immunostaining for YAP1 and LIFR in three cancer cell lines. Scale bars, 10 μm. c Western blot analysis of LIFR and p-YAP1 (S127) protein levels in WT and cLIF cancer cells transfected with SMARTpool LIFR siRNA or control siRNA. The p-YAP1 (S127) expressions with respect to total YAP1 levels were quantified and presented as mean ± SEM ( n = 3). At least three independent experiments were performed. d Western blot analysis of expression of focal adhesion molecules and SRC in WT and LIF +/− cancer cells transfected with YAP1 siRNA. GAPDH was used as the loading control. e Representative images for p-PXN (Y118) expression in WT or LIF +/− cancer cells transfected with YAP1 or control siRNA ( n = 3). Alexa Fluor 488 phalloidin (green) was used to stain F-actin. Scale bars, 10 μm. f Representative images of the HUVEC layer replacement assay. Fixed numbers of WT or LIF +/− cancer cells transfected with YAP1 or control siRNA were plated onto the confluent HUVEC layer and co-cultivated for 24 h. Cancer cells were labeled with antibody against pan-cytokeratin (red) and HUVEC cells with antibody against VE-cadherin (green). Scale bars, 20 μm. g , h Quantification of displaced areas depicted in f . WT cancer cells ( g ). LIF +/− cancer cells ( h ). Invaded areas were calculated using CellSens imaging software (Olympus). Data are presented with scatter dot plot (mean ± SEM). Each black dot represents one captured image. Mann–Whitney test. i Immunohistochemistry for LIFR and YAP1 expression (brown) in consecutive NPC biopsy sections derived from primary or bone marrow metastatic lesions

Journal: Nature Communications

Article Title: Cytoplasmic LIF reprograms invasive mode to enhance NPC dissemination through modulating YAP1-FAK/PXN signaling

doi: 10.1038/s41467-018-07660-6

Figure Lengend Snippet: LIFR–YAP1 signaling is critical for LIF-mediated invasion of NPC cells. a Endogenous protein expression of LIFR, p-YAP1(S127), and YAP1 in three cancer cell lines. b Immunostaining for YAP1 and LIFR in three cancer cell lines. Scale bars, 10 μm. c Western blot analysis of LIFR and p-YAP1 (S127) protein levels in WT and cLIF cancer cells transfected with SMARTpool LIFR siRNA or control siRNA. The p-YAP1 (S127) expressions with respect to total YAP1 levels were quantified and presented as mean ± SEM ( n = 3). At least three independent experiments were performed. d Western blot analysis of expression of focal adhesion molecules and SRC in WT and LIF +/− cancer cells transfected with YAP1 siRNA. GAPDH was used as the loading control. e Representative images for p-PXN (Y118) expression in WT or LIF +/− cancer cells transfected with YAP1 or control siRNA ( n = 3). Alexa Fluor 488 phalloidin (green) was used to stain F-actin. Scale bars, 10 μm. f Representative images of the HUVEC layer replacement assay. Fixed numbers of WT or LIF +/− cancer cells transfected with YAP1 or control siRNA were plated onto the confluent HUVEC layer and co-cultivated for 24 h. Cancer cells were labeled with antibody against pan-cytokeratin (red) and HUVEC cells with antibody against VE-cadherin (green). Scale bars, 20 μm. g , h Quantification of displaced areas depicted in f . WT cancer cells ( g ). LIF +/− cancer cells ( h ). Invaded areas were calculated using CellSens imaging software (Olympus). Data are presented with scatter dot plot (mean ± SEM). Each black dot represents one captured image. Mann–Whitney test. i Immunohistochemistry for LIFR and YAP1 expression (brown) in consecutive NPC biopsy sections derived from primary or bone marrow metastatic lesions

Techniques: Expressing, Immunostaining, Western Blot, Transfection, Control, Staining, Labeling, Imaging, Software, MANN-WHITNEY, Immunohistochemistry, Derivative Assay

AZD0530 treatment suppresses LIF-mediated tumor invasion. a Western blot analysis of YAP1 and focal adhesion proteins in cancer cells treated with AZD0530 (5 μM). Protein lysates were harvested at 24 h post treatment. b Immunostaining for YAP1 (red) in cancer cells treated with AZD0530. Alexa Fluor 488 phalloidin (green) was used to stain F-actin. Blue, nuclear staining. Scale bars, 10 μm. c – e Representative images of YAP1 ( c ), p-PXN (Y118) ( d ), and p-FAK (Y397) ( e ) expression in mouse WT and cLIF xenografts treated with AZD0530 or vehicle. Scale bars, 50 μm. f Quantification of mouse NPC xenografts with events of local invasion based on results of hematoxylin and eosin staining. The AZD0530 treatment procedure in the mouse model is described in Methods

Journal: Nature Communications

Article Title: Cytoplasmic LIF reprograms invasive mode to enhance NPC dissemination through modulating YAP1-FAK/PXN signaling

doi: 10.1038/s41467-018-07660-6

Figure Lengend Snippet: AZD0530 treatment suppresses LIF-mediated tumor invasion. a Western blot analysis of YAP1 and focal adhesion proteins in cancer cells treated with AZD0530 (5 μM). Protein lysates were harvested at 24 h post treatment. b Immunostaining for YAP1 (red) in cancer cells treated with AZD0530. Alexa Fluor 488 phalloidin (green) was used to stain F-actin. Blue, nuclear staining. Scale bars, 10 μm. c – e Representative images of YAP1 ( c ), p-PXN (Y118) ( d ), and p-FAK (Y397) ( e ) expression in mouse WT and cLIF xenografts treated with AZD0530 or vehicle. Scale bars, 50 μm. f Quantification of mouse NPC xenografts with events of local invasion based on results of hematoxylin and eosin staining. The AZD0530 treatment procedure in the mouse model is described in Methods

Techniques: Western Blot, Immunostaining, Staining, Expressing

AZD0530 treatment suppresses cancer vascular dissemination. a HUVEC layer replacement assay. Equal numbers of cancer cells were co-cultivated with confluent HUVEC cells for 24 h in the presence of AZD0530 (5 μm) or vehicle (DMSO). Cells were fixed and labeled with antibodies against pan-cytokeratin (red) and VE-cadherin (green). Scale bars, 20 μm. Blue, nuclear staining. b – d Quantification of displaced areas described in a . HUVEC + WT cancer cells ( b ). HUVEC + LIF +/− cancer cells ( c ). HUVEC + cLIF cancer cells ( d ). Invaded areas were calculated using CellSens imaging software (Olympus). Data are presented with scatter dot plot (mean ± SEM). Each black dot represents one captured image. ** p < 0.01, *** p < 0.001, Mann–Whitney test. e Western blot analysis of p-YAP, VE-cadherin, and CD31 expression in co-cultivated cancer cells and HUVEC cells, as described in a . Total protein lysates were harvested 24 h post AZD0530 treatment using GAPDH as a loading control. f – h Quantification of disseminated tumor-like structures in zebrafish embryonic xenograft models. WT xenografts ( f ). LIF +/− xenografts ( g ). cLIF xenografts ( h ). The number of disseminated tumor-like structures was determined on day 4 after treatment with AZD0530 (15 μm) or vehicle (DMSO). Data are presented with scatter dot plot (mean ± SEM). Each black dot represents one fish embryo. ** p < 0.01, *** p < 0.001, Mann–Whitney test

Journal: Nature Communications

Article Title: Cytoplasmic LIF reprograms invasive mode to enhance NPC dissemination through modulating YAP1-FAK/PXN signaling

doi: 10.1038/s41467-018-07660-6

Figure Lengend Snippet: AZD0530 treatment suppresses cancer vascular dissemination. a HUVEC layer replacement assay. Equal numbers of cancer cells were co-cultivated with confluent HUVEC cells for 24 h in the presence of AZD0530 (5 μm) or vehicle (DMSO). Cells were fixed and labeled with antibodies against pan-cytokeratin (red) and VE-cadherin (green). Scale bars, 20 μm. Blue, nuclear staining. b – d Quantification of displaced areas described in a . HUVEC + WT cancer cells ( b ). HUVEC + LIF +/− cancer cells ( c ). HUVEC + cLIF cancer cells ( d ). Invaded areas were calculated using CellSens imaging software (Olympus). Data are presented with scatter dot plot (mean ± SEM). Each black dot represents one captured image. ** p < 0.01, *** p < 0.001, Mann–Whitney test. e Western blot analysis of p-YAP, VE-cadherin, and CD31 expression in co-cultivated cancer cells and HUVEC cells, as described in a . Total protein lysates were harvested 24 h post AZD0530 treatment using GAPDH as a loading control. f – h Quantification of disseminated tumor-like structures in zebrafish embryonic xenograft models. WT xenografts ( f ). LIF +/− xenografts ( g ). cLIF xenografts ( h ). The number of disseminated tumor-like structures was determined on day 4 after treatment with AZD0530 (15 μm) or vehicle (DMSO). Data are presented with scatter dot plot (mean ± SEM). Each black dot represents one fish embryo. ** p < 0.01, *** p < 0.001, Mann–Whitney test

Techniques: Labeling, Staining, Imaging, Software, MANN-WHITNEY, Western Blot, Expressing, Control

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