listing of every known paper relating to field flow fractionation Search Results


hcd33 him3-4 antibody  (Becton Dickinson)
90
Becton Dickinson hcd33 him3-4 antibody
Hcd33 Him3 4 Antibody, supplied by Becton Dickinson, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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rabbit polyclonal anti ncl antibody  (Cell Signaling Technology Inc)
95
Cell Signaling Technology Inc rabbit polyclonal anti ncl antibody
Rabbit Polyclonal Anti Ncl Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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flow cytometry staining buffer  (Thermo Fisher)
98
Thermo Fisher flow cytometry staining buffer
Flow Cytometry Staining Buffer, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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flow cytometry staining buffer - by Bioz Stars, 2026-11
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vector” pecvd module  (Novellus Systems Inc)
90
Novellus Systems Inc vector” pecvd module
Vector” Pecvd Module, supplied by Novellus Systems Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 90 stars, based on 1 article reviews
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partek flow v4 0  (Partek)
86
Partek partek flow v4 0
Partek Flow V4 0, supplied by Partek, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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flow cytometry list behavior enumeratedprefix word mark type decimalmax label size  (Eppendorf AG)
96
Eppendorf AG flow cytometry list behavior enumeratedprefix word mark type decimalmax label size
Flow Cytometry List Behavior Enumeratedprefix Word Mark Type Decimalmax Label Size, supplied by Eppendorf AG, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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p fgfr1 tyr653 654 mouse mab  (Cell Signaling Technology Inc)
94
Cell Signaling Technology Inc p fgfr1 tyr653 654 mouse mab
DJ-1 induced <t>FGFR1</t> 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.
P Fgfr1 Tyr653 654 Mouse Mab, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/listing+of+every+known+paper+relating+to+field+flow+fractionation/Phospho-FGF+Receptor+(Tyr653%2F654)+Mouse+mAb/pmc09236769-74-6-13
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antibodies against α tubulin hrp conjugated  (Proteintech)
96
Proteintech antibodies against α tubulin hrp conjugated
Deregulation of Bcl-2 proteins mediates KPNB1 inhibition-induced apoptosis in glioblastoma cells. a Total Bax, active Bax, total Bak, and active Bak were immunoprecipitated from control and shKPNB1-U87 and U251 cells, respectively. Interaction proteins were identified by western blots. b Mcl-1 and Bcl-xL were immunoprecipitated from IPZ (16 μM)-treated U87 and U251 cells, followed by western blots. c , d U87 and U251 cells were infected with lentiviruses encoding shKPNB1s and/or Bcl-xL (S62A). c Western blots analysis of the cytosolic and mitochondrial proteins in U87 cells. d The sub-G1 population analysis ( n = 2, mean ± s.d., * P < 0.05) and western blots in U87 and U251 cells. e U87 and U251 cells were infected with lentiviruses encoding shKPNB1s and/or Mcl-1 (T92A), followed by the sub-G1 population analysis ( n = 2, mean ± s.d., * P < 0.05) and western blots. f U87 and U251 cells expressing Bcl-xL (S62A) or Mcl-1 (T92A) were treated with IPZ (16 μM), followed by sub-G1 population analysis ( n = 2, mean ± s.d., * P < 0.05). g U87 and U251 cells were infected with lentiviruses as indicated, followed by the sub-G1 population analysis ( n = 2, mean ± s.d., * P < 0.05, compared with respective shKPNB1 group) and western blots. h U87 and U251 cells expressing shBax and/or shBak were treated with IPZ (16 μM), followed by sub-G1 population analysis ( n = 3, mean ± s.d., * P < 0.05). i U87 and U251 cells were infected with lentiviruses as indicated, followed by the sub-G1 population analysis ( n = 3, mean ± s.d., * P < 0.05, compared with respective shKPNB1 group) and western blots. j U87 and U251 cells expressing shNoxa and/or shPuma were treated with IPZ (16 μM), followed by sub-G1 population analysis ( n = 3, mean ± s.d., * P < 0.05). For western blots, <t>GAPDH,</t> <t>α-tubulin,</t> and COX4 were used as the loading control of total cell lysate, cytosol fraction, and mitochondria fraction, respectively
Antibodies Against α Tubulin Hrp Conjugated, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/listing+of+every+known+paper+relating+to+field+flow+fractionation/HRP-conjugated+alpha+Tubulin+Antibody/pmc05978811-209-9-26
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incubation with sepharose  (Danaher Inc)
94
Danaher Inc incubation with sepharose
Deregulation of Bcl-2 proteins mediates KPNB1 inhibition-induced apoptosis in glioblastoma cells. a Total Bax, active Bax, total Bak, and active Bak were immunoprecipitated from control and shKPNB1-U87 and U251 cells, respectively. Interaction proteins were identified by western blots. b Mcl-1 and Bcl-xL were immunoprecipitated from IPZ (16 μM)-treated U87 and U251 cells, followed by western blots. c , d U87 and U251 cells were infected with lentiviruses encoding shKPNB1s and/or Bcl-xL (S62A). c Western blots analysis of the cytosolic and mitochondrial proteins in U87 cells. d The sub-G1 population analysis ( n = 2, mean ± s.d., * P < 0.05) and western blots in U87 and U251 cells. e U87 and U251 cells were infected with lentiviruses encoding shKPNB1s and/or Mcl-1 (T92A), followed by the sub-G1 population analysis ( n = 2, mean ± s.d., * P < 0.05) and western blots. f U87 and U251 cells expressing Bcl-xL (S62A) or Mcl-1 (T92A) were treated with IPZ (16 μM), followed by sub-G1 population analysis ( n = 2, mean ± s.d., * P < 0.05). g U87 and U251 cells were infected with lentiviruses as indicated, followed by the sub-G1 population analysis ( n = 2, mean ± s.d., * P < 0.05, compared with respective shKPNB1 group) and western blots. h U87 and U251 cells expressing shBax and/or shBak were treated with IPZ (16 μM), followed by sub-G1 population analysis ( n = 3, mean ± s.d., * P < 0.05). i U87 and U251 cells were infected with lentiviruses as indicated, followed by the sub-G1 population analysis ( n = 3, mean ± s.d., * P < 0.05, compared with respective shKPNB1 group) and western blots. j U87 and U251 cells expressing shNoxa and/or shPuma were treated with IPZ (16 μM), followed by sub-G1 population analysis ( n = 3, mean ± s.d., * P < 0.05). For western blots, <t>GAPDH,</t> <t>α-tubulin,</t> and COX4 were used as the loading control of total cell lysate, cytosol fraction, and mitochondria fraction, respectively
Incubation With Sepharose, supplied by Danaher Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/listing+of+every+known+paper+relating+to+field+flow+fractionation/Protein+G+Sepharose+4+Fast+Flow/pm27521426-257-13-16
Average 94 stars, based on 1 article reviews
incubation with sepharose - by Bioz Stars, 2026-11
94/100 stars
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fisher miltenyi biotec cat 130 059 901  (Miltenyi Biotec)
97
Miltenyi Biotec fisher miltenyi biotec cat 130 059 901
Deregulation of Bcl-2 proteins mediates KPNB1 inhibition-induced apoptosis in glioblastoma cells. a Total Bax, active Bax, total Bak, and active Bak were immunoprecipitated from control and shKPNB1-U87 and U251 cells, respectively. Interaction proteins were identified by western blots. b Mcl-1 and Bcl-xL were immunoprecipitated from IPZ (16 μM)-treated U87 and U251 cells, followed by western blots. c , d U87 and U251 cells were infected with lentiviruses encoding shKPNB1s and/or Bcl-xL (S62A). c Western blots analysis of the cytosolic and mitochondrial proteins in U87 cells. d The sub-G1 population analysis ( n = 2, mean ± s.d., * P < 0.05) and western blots in U87 and U251 cells. e U87 and U251 cells were infected with lentiviruses encoding shKPNB1s and/or Mcl-1 (T92A), followed by the sub-G1 population analysis ( n = 2, mean ± s.d., * P < 0.05) and western blots. f U87 and U251 cells expressing Bcl-xL (S62A) or Mcl-1 (T92A) were treated with IPZ (16 μM), followed by sub-G1 population analysis ( n = 2, mean ± s.d., * P < 0.05). g U87 and U251 cells were infected with lentiviruses as indicated, followed by the sub-G1 population analysis ( n = 2, mean ± s.d., * P < 0.05, compared with respective shKPNB1 group) and western blots. h U87 and U251 cells expressing shBax and/or shBak were treated with IPZ (16 μM), followed by sub-G1 population analysis ( n = 3, mean ± s.d., * P < 0.05). i U87 and U251 cells were infected with lentiviruses as indicated, followed by the sub-G1 population analysis ( n = 3, mean ± s.d., * P < 0.05, compared with respective shKPNB1 group) and western blots. j U87 and U251 cells expressing shNoxa and/or shPuma were treated with IPZ (16 μM), followed by sub-G1 population analysis ( n = 3, mean ± s.d., * P < 0.05). For western blots, <t>GAPDH,</t> <t>α-tubulin,</t> and COX4 were used as the loading control of total cell lysate, cytosol fraction, and mitochondria fraction, respectively
Fisher Miltenyi Biotec Cat 130 059 901, supplied by Miltenyi Biotec, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/listing+of+every+known+paper+relating+to+field+flow+fractionation/FcR+Blocking+Reagent%2C+human/pmc06082021-636-9-9
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fisher miltenyi biotec cat 130 059 901 - by Bioz Stars, 2026-11
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fortessa flow cytometer  (Becton Dickinson)
90
Becton Dickinson fortessa flow cytometer
Deregulation of Bcl-2 proteins mediates KPNB1 inhibition-induced apoptosis in glioblastoma cells. a Total Bax, active Bax, total Bak, and active Bak were immunoprecipitated from control and shKPNB1-U87 and U251 cells, respectively. Interaction proteins were identified by western blots. b Mcl-1 and Bcl-xL were immunoprecipitated from IPZ (16 μM)-treated U87 and U251 cells, followed by western blots. c , d U87 and U251 cells were infected with lentiviruses encoding shKPNB1s and/or Bcl-xL (S62A). c Western blots analysis of the cytosolic and mitochondrial proteins in U87 cells. d The sub-G1 population analysis ( n = 2, mean ± s.d., * P < 0.05) and western blots in U87 and U251 cells. e U87 and U251 cells were infected with lentiviruses encoding shKPNB1s and/or Mcl-1 (T92A), followed by the sub-G1 population analysis ( n = 2, mean ± s.d., * P < 0.05) and western blots. f U87 and U251 cells expressing Bcl-xL (S62A) or Mcl-1 (T92A) were treated with IPZ (16 μM), followed by sub-G1 population analysis ( n = 2, mean ± s.d., * P < 0.05). g U87 and U251 cells were infected with lentiviruses as indicated, followed by the sub-G1 population analysis ( n = 2, mean ± s.d., * P < 0.05, compared with respective shKPNB1 group) and western blots. h U87 and U251 cells expressing shBax and/or shBak were treated with IPZ (16 μM), followed by sub-G1 population analysis ( n = 3, mean ± s.d., * P < 0.05). i U87 and U251 cells were infected with lentiviruses as indicated, followed by the sub-G1 population analysis ( n = 3, mean ± s.d., * P < 0.05, compared with respective shKPNB1 group) and western blots. j U87 and U251 cells expressing shNoxa and/or shPuma were treated with IPZ (16 μM), followed by sub-G1 population analysis ( n = 3, mean ± s.d., * P < 0.05). For western blots, <t>GAPDH,</t> <t>α-tubulin,</t> and COX4 were used as the loading control of total cell lysate, cytosol fraction, and mitochondria fraction, respectively
Fortessa Flow Cytometer, supplied by Becton Dickinson, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/listing+of+every+known+paper+relating+to+field+flow+fractionation/fortessa+flow+cytometer/us10428305-231-15-22
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fortessa flow cytometer - by Bioz Stars, 2026-11
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cd45 buv395  (Becton Dickinson)
90
Becton Dickinson cd45 buv395
Deregulation of Bcl-2 proteins mediates KPNB1 inhibition-induced apoptosis in glioblastoma cells. a Total Bax, active Bax, total Bak, and active Bak were immunoprecipitated from control and shKPNB1-U87 and U251 cells, respectively. Interaction proteins were identified by western blots. b Mcl-1 and Bcl-xL were immunoprecipitated from IPZ (16 μM)-treated U87 and U251 cells, followed by western blots. c , d U87 and U251 cells were infected with lentiviruses encoding shKPNB1s and/or Bcl-xL (S62A). c Western blots analysis of the cytosolic and mitochondrial proteins in U87 cells. d The sub-G1 population analysis ( n = 2, mean ± s.d., * P < 0.05) and western blots in U87 and U251 cells. e U87 and U251 cells were infected with lentiviruses encoding shKPNB1s and/or Mcl-1 (T92A), followed by the sub-G1 population analysis ( n = 2, mean ± s.d., * P < 0.05) and western blots. f U87 and U251 cells expressing Bcl-xL (S62A) or Mcl-1 (T92A) were treated with IPZ (16 μM), followed by sub-G1 population analysis ( n = 2, mean ± s.d., * P < 0.05). g U87 and U251 cells were infected with lentiviruses as indicated, followed by the sub-G1 population analysis ( n = 2, mean ± s.d., * P < 0.05, compared with respective shKPNB1 group) and western blots. h U87 and U251 cells expressing shBax and/or shBak were treated with IPZ (16 μM), followed by sub-G1 population analysis ( n = 3, mean ± s.d., * P < 0.05). i U87 and U251 cells were infected with lentiviruses as indicated, followed by the sub-G1 population analysis ( n = 3, mean ± s.d., * P < 0.05, compared with respective shKPNB1 group) and western blots. j U87 and U251 cells expressing shNoxa and/or shPuma were treated with IPZ (16 μM), followed by sub-G1 population analysis ( n = 3, mean ± s.d., * P < 0.05). For western blots, <t>GAPDH,</t> <t>α-tubulin,</t> and COX4 were used as the loading control of total cell lysate, cytosol fraction, and mitochondria fraction, respectively
Cd45 Buv395, supplied by Becton Dickinson, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/listing+of+every+known+paper+relating+to+field+flow+fractionation/anti+cd3/pmc09133109__41467_2022_30467_MOESM2_ESM-47-9-14
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Image Search Results


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.

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

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).

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

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.

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

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.

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

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.

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

Deregulation of Bcl-2 proteins mediates KPNB1 inhibition-induced apoptosis in glioblastoma cells. a Total Bax, active Bax, total Bak, and active Bak were immunoprecipitated from control and shKPNB1-U87 and U251 cells, respectively. Interaction proteins were identified by western blots. b Mcl-1 and Bcl-xL were immunoprecipitated from IPZ (16 μM)-treated U87 and U251 cells, followed by western blots. c , d U87 and U251 cells were infected with lentiviruses encoding shKPNB1s and/or Bcl-xL (S62A). c Western blots analysis of the cytosolic and mitochondrial proteins in U87 cells. d The sub-G1 population analysis ( n = 2, mean ± s.d., * P < 0.05) and western blots in U87 and U251 cells. e U87 and U251 cells were infected with lentiviruses encoding shKPNB1s and/or Mcl-1 (T92A), followed by the sub-G1 population analysis ( n = 2, mean ± s.d., * P < 0.05) and western blots. f U87 and U251 cells expressing Bcl-xL (S62A) or Mcl-1 (T92A) were treated with IPZ (16 μM), followed by sub-G1 population analysis ( n = 2, mean ± s.d., * P < 0.05). g U87 and U251 cells were infected with lentiviruses as indicated, followed by the sub-G1 population analysis ( n = 2, mean ± s.d., * P < 0.05, compared with respective shKPNB1 group) and western blots. h U87 and U251 cells expressing shBax and/or shBak were treated with IPZ (16 μM), followed by sub-G1 population analysis ( n = 3, mean ± s.d., * P < 0.05). i U87 and U251 cells were infected with lentiviruses as indicated, followed by the sub-G1 population analysis ( n = 3, mean ± s.d., * P < 0.05, compared with respective shKPNB1 group) and western blots. j U87 and U251 cells expressing shNoxa and/or shPuma were treated with IPZ (16 μM), followed by sub-G1 population analysis ( n = 3, mean ± s.d., * P < 0.05). For western blots, GAPDH, α-tubulin, and COX4 were used as the loading control of total cell lysate, cytosol fraction, and mitochondria fraction, respectively

Journal: Oncogene

Article Title: KPNB1 inhibition disrupts proteostasis and triggers unfolded protein response-mediated apoptosis in glioblastoma cells

doi: 10.1038/s41388-018-0180-9

Figure Lengend Snippet: Deregulation of Bcl-2 proteins mediates KPNB1 inhibition-induced apoptosis in glioblastoma cells. a Total Bax, active Bax, total Bak, and active Bak were immunoprecipitated from control and shKPNB1-U87 and U251 cells, respectively. Interaction proteins were identified by western blots. b Mcl-1 and Bcl-xL were immunoprecipitated from IPZ (16 μM)-treated U87 and U251 cells, followed by western blots. c , d U87 and U251 cells were infected with lentiviruses encoding shKPNB1s and/or Bcl-xL (S62A). c Western blots analysis of the cytosolic and mitochondrial proteins in U87 cells. d The sub-G1 population analysis ( n = 2, mean ± s.d., * P < 0.05) and western blots in U87 and U251 cells. e U87 and U251 cells were infected with lentiviruses encoding shKPNB1s and/or Mcl-1 (T92A), followed by the sub-G1 population analysis ( n = 2, mean ± s.d., * P < 0.05) and western blots. f U87 and U251 cells expressing Bcl-xL (S62A) or Mcl-1 (T92A) were treated with IPZ (16 μM), followed by sub-G1 population analysis ( n = 2, mean ± s.d., * P < 0.05). g U87 and U251 cells were infected with lentiviruses as indicated, followed by the sub-G1 population analysis ( n = 2, mean ± s.d., * P < 0.05, compared with respective shKPNB1 group) and western blots. h U87 and U251 cells expressing shBax and/or shBak were treated with IPZ (16 μM), followed by sub-G1 population analysis ( n = 3, mean ± s.d., * P < 0.05). i U87 and U251 cells were infected with lentiviruses as indicated, followed by the sub-G1 population analysis ( n = 3, mean ± s.d., * P < 0.05, compared with respective shKPNB1 group) and western blots. j U87 and U251 cells expressing shNoxa and/or shPuma were treated with IPZ (16 μM), followed by sub-G1 population analysis ( n = 3, mean ± s.d., * P < 0.05). For western blots, GAPDH, α-tubulin, and COX4 were used as the loading control of total cell lysate, cytosol fraction, and mitochondria fraction, respectively

Article Snippet: Primary antibodies used in this study were listed below: antibodies against α-tubulin (HRP-conjugated) (HRP-66031), BubR1 (11504-2-AP), CD133 (18470-1-AP), GFAP (6190-1-Ig), KPNB1 (10077-1-AP), MAD2 (10337-1-AP), Tuj1 (10094-1-AP) (ProteinTech Group, Wuhan, China), p-IRE1α (S724) (ab124945), ubiquitin (Alexa Fluor 647) (ab205468) (Abcam, Canbridge, UK), ATF4 (11815), ATF6 (65880), Atg3 (3415), Atg5 (12994), Atg7 (8558), Bax (5023), Bak (12105), Bcl-2 (4223), Bcl-xL (2764), Bim (2933), calnexin (2679), caspase-3 (9662), CHIP (2080), CHOP (2895), Histone H3 (3377), HSC70/HSPA8 (8444), HSP70 (4872), HSP90 (4877), LC3B (3868), Mcl-1 (5453), MeCP2 (3456), Noxa (14766), Oct4 (2750), p62 (8025), p62 (Alexa Fluor 488) (8833), NF-kB p65 (8242), PARP (9532), p-Aurora A (T288)/Aurora B (T232)/Aurora C (T198) (2914), p-Histone H3 (S10) (4499), p-PERK (T980) (3179), Puma (12450), ubiquitin (HRP-conjugated) (14049), XBP1s (12782) (Cell Signaling Technology, Beverly, USA), Bax (6A7) (556467), Mcl-1 (for immunoprecipitation) (559027) (BD Biosciences, San Jose, USA), Bak, NT (06-536) (Merck Millipore, Darmstadt, Germany), ATF3 (BS2261), cyclin B1 (BS1392), eIF2α (BS3651), p27 (BS3714), p-Bcl-xL (S62) (BS4025), p-eIF2α (S51) (BS4787), PERK (BS2156) (Bioworld Technology, Nanjing, China), CDC2 (AF0778), p-CDC2 (T161) (AF8001) (Affinity Biologicals, Zhenjiang City, China), and GAPDH (KC-5G5) (Kangchen, Shanghai, China).

Techniques: Inhibition, Immunoprecipitation, Control, Western Blot, Infection, Expressing

Proteostasis perturbation and UPR upon KPNB1 inhibition dictate glioblastoma cell apoptosis. a Western blots analysis of cytosolic and nuclear p65 level in IPZ (16 μM)-treated U87 cells. b p65 was immunoprecipitated from IPZ (16 μM)-treated or INI-43 (8 μM)-treated U87 and U251 cells, followed by western blots. c U87 and U251 treated with IPZ (16 μM) were harvested at indicated time points before western blots. d Representative images showing p62 and ubiquitin staining in IPZ (16 μM)-treated U87 and U251 cells. Magnification, ×60; scale bar, 10 μm. e Representative images showing p62, p65, and ubiquitin staining in IPZ (16 μM)-treated U87 and U251 cells. Arrows indicate colocalization of p62, p65, and ubiquitin. Magnification, ×60; scale bar, 10 μm. f U87 and U251 cells were treated with IPZ at indicated concentrations for 24 h and subjected to western blots. g C6 cells and rat astrocytes were treated with IPZ at indicated concentrations for 48 h and subjected to western blots. h U87 and U251 cells overexpressing KPNB1-3Flag were treated with IPZ (16 μM) for indicated times and subjected to western blots. i U87 and U251 cells treated with IPZ (16 μM) were treated with Act D (0.5 μg/ml) or CHX (U87: 0.5 μg/ml and U251: 2.5 μg/ml) and subjected to western blots. j U87 and U251 cells were treated with or without IPZ (16 μM) and CHX and subjected to flow cytometry ( n = 2, mean ± s.d., * P < 0.05) and western blots. k Western blots analysis of cytosolic and nuclear levels of ATF4, CHOP, and ATF3 in IPZ (16 μM)-treated U87 cells. l U87 and U251 cells expressing shATF4, shCHOP, or shATF3 were treated with IPZ (16 μM) and subjected to flow cytometry ( n = 2, mean ± s.d., * P < 0.05) and western blots. For western blots, α-tubulin, MeCP2, and GAPDH were used as the loading control of cytosol fraction, mitochondria fraction, and total cell lysate, respectively

Journal: Oncogene

Article Title: KPNB1 inhibition disrupts proteostasis and triggers unfolded protein response-mediated apoptosis in glioblastoma cells

doi: 10.1038/s41388-018-0180-9

Figure Lengend Snippet: Proteostasis perturbation and UPR upon KPNB1 inhibition dictate glioblastoma cell apoptosis. a Western blots analysis of cytosolic and nuclear p65 level in IPZ (16 μM)-treated U87 cells. b p65 was immunoprecipitated from IPZ (16 μM)-treated or INI-43 (8 μM)-treated U87 and U251 cells, followed by western blots. c U87 and U251 treated with IPZ (16 μM) were harvested at indicated time points before western blots. d Representative images showing p62 and ubiquitin staining in IPZ (16 μM)-treated U87 and U251 cells. Magnification, ×60; scale bar, 10 μm. e Representative images showing p62, p65, and ubiquitin staining in IPZ (16 μM)-treated U87 and U251 cells. Arrows indicate colocalization of p62, p65, and ubiquitin. Magnification, ×60; scale bar, 10 μm. f U87 and U251 cells were treated with IPZ at indicated concentrations for 24 h and subjected to western blots. g C6 cells and rat astrocytes were treated with IPZ at indicated concentrations for 48 h and subjected to western blots. h U87 and U251 cells overexpressing KPNB1-3Flag were treated with IPZ (16 μM) for indicated times and subjected to western blots. i U87 and U251 cells treated with IPZ (16 μM) were treated with Act D (0.5 μg/ml) or CHX (U87: 0.5 μg/ml and U251: 2.5 μg/ml) and subjected to western blots. j U87 and U251 cells were treated with or without IPZ (16 μM) and CHX and subjected to flow cytometry ( n = 2, mean ± s.d., * P < 0.05) and western blots. k Western blots analysis of cytosolic and nuclear levels of ATF4, CHOP, and ATF3 in IPZ (16 μM)-treated U87 cells. l U87 and U251 cells expressing shATF4, shCHOP, or shATF3 were treated with IPZ (16 μM) and subjected to flow cytometry ( n = 2, mean ± s.d., * P < 0.05) and western blots. For western blots, α-tubulin, MeCP2, and GAPDH were used as the loading control of cytosol fraction, mitochondria fraction, and total cell lysate, respectively

Article Snippet: Primary antibodies used in this study were listed below: antibodies against α-tubulin (HRP-conjugated) (HRP-66031), BubR1 (11504-2-AP), CD133 (18470-1-AP), GFAP (6190-1-Ig), KPNB1 (10077-1-AP), MAD2 (10337-1-AP), Tuj1 (10094-1-AP) (ProteinTech Group, Wuhan, China), p-IRE1α (S724) (ab124945), ubiquitin (Alexa Fluor 647) (ab205468) (Abcam, Canbridge, UK), ATF4 (11815), ATF6 (65880), Atg3 (3415), Atg5 (12994), Atg7 (8558), Bax (5023), Bak (12105), Bcl-2 (4223), Bcl-xL (2764), Bim (2933), calnexin (2679), caspase-3 (9662), CHIP (2080), CHOP (2895), Histone H3 (3377), HSC70/HSPA8 (8444), HSP70 (4872), HSP90 (4877), LC3B (3868), Mcl-1 (5453), MeCP2 (3456), Noxa (14766), Oct4 (2750), p62 (8025), p62 (Alexa Fluor 488) (8833), NF-kB p65 (8242), PARP (9532), p-Aurora A (T288)/Aurora B (T232)/Aurora C (T198) (2914), p-Histone H3 (S10) (4499), p-PERK (T980) (3179), Puma (12450), ubiquitin (HRP-conjugated) (14049), XBP1s (12782) (Cell Signaling Technology, Beverly, USA), Bax (6A7) (556467), Mcl-1 (for immunoprecipitation) (559027) (BD Biosciences, San Jose, USA), Bak, NT (06-536) (Merck Millipore, Darmstadt, Germany), ATF3 (BS2261), cyclin B1 (BS1392), eIF2α (BS3651), p27 (BS3714), p-Bcl-xL (S62) (BS4025), p-eIF2α (S51) (BS4787), PERK (BS2156) (Bioworld Technology, Nanjing, China), CDC2 (AF0778), p-CDC2 (T161) (AF8001) (Affinity Biologicals, Zhenjiang City, China), and GAPDH (KC-5G5) (Kangchen, Shanghai, China).

Techniques: Inhibition, Western Blot, Immunoprecipitation, Ubiquitin Proteomics, Staining, Flow Cytometry, Expressing, Control