Journal: International Journal of Clinical and Experimental Pathology

Article Title: Dioscin ameliorates peritoneal fibrosis by inhibiting epithelial-to-mesenchymal transition of human peritoneal mesothelial cells via the TLR4/MyD88/NF-κB signaling pathway

doi:

Figure Lengend Snippet: Dioscin inhibits LPS-induced fibrosis in HMrSV5 cells. Western blotting for detecting protein levels of α-SMA, collagen I and fibronectin. ###P < 0.001 compared with negative control group or dioscin (1.0 μg/ml) group. ***P < 0.001 compared with LPS group. NC, negative control; LPS, lipopolysaccharide; Dio, Dioscin; α-SMA, α-smooth muscle actin.

Article Snippet: Then the membranes were incubated with following primary antibodies: α-SMA (1:100, Proteintech Group), collagen I (1:100, Proteintech Group), fibronectin (1:250, Abcam), TLR4 (1:1000, Proteintech Group), MyD88 (1:1000, Proteintech Group), NF-κB (1:1000, Proteintech Group), TGF-β1 (1:1000, Proteintech Group), p-Smad2/Smad2 (1:1000, Proteintech Group), respectively.

Techniques: Western Blot, Negative Control

Journal: International Journal of Clinical and Experimental Pathology

Article Title: Dioscin ameliorates peritoneal fibrosis by inhibiting epithelial-to-mesenchymal transition of human peritoneal mesothelial cells via the TLR4/MyD88/NF-κB signaling pathway

doi:

Figure Lengend Snippet: Dioscin inhibits EMT and fibrosis through TLR4/MyD88/NF-κB pathway in HMrSV5 cells. A. Western blotting for assessing protein levels of TLR4, MyD88, NF-κB, TGF-β1, p-Smad2, Smad2, α-SMA, collagen I and fibronectin. B. immunofluorescence assay for detecting expressions of α-SMA, collagen I and fibronectin in LPS+TLR4 group and LPS+TLR4+dioscin (0.5 μg/ml) group. ###P < 0.001 compared with negative control group or Ppicza group. *P < 0.05, **P < 0.01 and ***P < 0.001 compared with LPS+ pPICZA group or LPS+TLR4 group. NC, negative control; LPS, lipopolysaccharide; Dio, Dioscin; α-SMA, α-smooth muscle actin; MyD88, myeloid differentiation factor 88; NF-κB, nuclear factor κB; TGF-β1, transforming growth factor-β1; TLR4, Toll-like receptor (TLR) 4.

Article Snippet: Then the membranes were incubated with following primary antibodies: α-SMA (1:100, Proteintech Group), collagen I (1:100, Proteintech Group), fibronectin (1:250, Abcam), TLR4 (1:1000, Proteintech Group), MyD88 (1:1000, Proteintech Group), NF-κB (1:1000, Proteintech Group), TGF-β1 (1:1000, Proteintech Group), p-Smad2/Smad2 (1:1000, Proteintech Group), respectively.

Techniques: Western Blot, Immunofluorescence, Negative Control

Journal: Ecotoxicology and environmental safety

Article Title: Hexavalent chromium triggers hepatocytes premature senescence via the GATA4/NF-κB signaling pathway mediated by the DNA damage response.

doi: 10.1016/j.ecoenv.2022.113645

Figure Lengend Snippet: Fig. 1. Cr(VI) triggered premature senescence in L02 hepatocytes accompanied with increased GATA4 expression. The cells were exposed to PBS or 10 nM Cr (VI) 3 times a week for 24 h for 4 consecutive weeks. (A) The morphology detection showed that Cr(VI)-treated cells were enlarged, flattened and more vacuolized (magnification: 20 ×). (B) The development of hepatocytes senescence was examined by SA-β-gal staining. (C) The senescence-associated proteins including FN1, CLU and SMP30 were detected by western blotting. (D-E) Dynamic changes during premature senescence development after Cr(VI) exposure, including morpho logical changes as well as SA-β-gal staining (magnification:20 ×). (F) The expression level of GATA4 was determined using western blotting. * p < 0.05, * * p < 0.01, * ** p < 0.001, compared with control.

Article Snippet: Primary antibodies of Fibronectin 1 (FN1) (15613–1-AP), GATA4 (19530–1-AP), TRAF3 Interacting Protein 2 (TRAF3IP2) (26692–1-AP), Y. Ma et al. Ecotoxicology and Environmental Safety 239 (2022) 113645 Y. Ma et al. Ecotoxicology and Environmental Safety 239 (2022) 113645 NF-κB (p65) (10745–1-AP), and senescence marker protein-30 (SMP30) (17947–1-AP) were purchased from proteintech (Wuhan, China); Phospho-NF-κB p65 (p-p65) (Ser536) (93H1), IκBα (44D4), PhosphoIκBα (p-IκBα) (Ser32) (14D4), Atg5 (D5G3) and Atg7 (D12B11) were obtained from Cell Signaling Technology (MA, USA).

Techniques: Expressing, Staining, Western Blot, Control

Journal: Theranostics

Article Title: Exosomal miR-21 from tubular cells contributes to renal fibrosis by activating fibroblasts via targeting PTEN in obstructed kidneys

doi: 10.7150/thno.62820

Figure Lengend Snippet: TGF-β1 expression and exosome production are increased in UUO-induced renal fibrosis models. (A-C) Representative micrographs of immunohistochemical staining (A) and quantitative data (B,C) show TGF-β1 and Collagen I expression at different time points after UUO. Scales bars = 50μm. * p < 0.05 versus sham, # p < 0.05 versus UUO-3d (n = 6). (D-F) Representative micrographs of Masson staining and Sirius red staining (D) and quantitative data (E, F) show collagen fiber accumulation after UUO. Scales bars=50 μm. * p < 0.05 versus sham, # p < 0.05 versus UUO-3d (n = 6). (G, H) Representative western blot (G) and quantitative data (H) on TGF-β1, fibronectin and exosomal-specific proteins CD63 and TSG101 after UUO. Numbers (1 to 3) indicate each individual animal in the given group. * p < 0.05 versus sham, # p < 0.05 versus UUO-3d (n = 6). (I) Transmission electron microscopy (TEM) shows the exosomes and microvesicles released by renal tubular epithelial cells after UUO. Scales bars = 300 nm. (J) Double immunofluorescence staining (green for CD63 and red for TSG101) demonstrates the generation of exosomes predominantly in tubular epithelial cells after UUO. Scales bars = 5 μm. (K, L) Quantitative determination of CD63- and TSG101-positive renal tubules. Data were obtained from 3 images per mouse, with 6 mice per group. * p < 0.05 versus sham, # p < 0.05 versus UUO-3d.

Article Snippet: The primary antibodies were as follows: TGF-β1 (Sigma, SAB4502954), CD63 (Affinity Biosciences, AF5117), TSG-101 (Abcam, ab125011), Fibronectin (Proteintech Group, 15613-1-AP), α-SMA (Boster Biological Technology, BM0002), Collagen I (Novus Biologicals, NB600-408), E-cadherin (Abcam, ab76319), Fsp-1 (Cell Signaling Technology, 13018), PCNA (Abcam, ab92552), PTEN (Cell Signaling Technology, 9559), and p-Akt (Abcam, ab18785).

Techniques: Expressing, Immunohistochemical staining, Staining, Western Blot, Transmission Assay, Electron Microscopy, Double Immunofluorescence Staining

Journal: Theranostics

Article Title: Exosomal miR-21 from tubular cells contributes to renal fibrosis by activating fibroblasts via targeting PTEN in obstructed kidneys

doi: 10.7150/thno.62820

Figure Lengend Snippet: TGF-β1 promotes the secretion of exosomes by renal tubular epithelial cells and activates fibroblasts in vitro . (A) Schematic diagram of experimental process. Exosomes from NRK-52E cells treated without (Ctrl-Exos) or with TGF-β1 (TGFβ1-Exos) were extracted and incubated with NRK-49F cells. (B,C) DLS and NTA of exosomes from NRK-52E cells. (D) TEM image of exosomes isolated from NRK-52E cells. Scale bar = 100 nm. (E, F) Representative western blot (E) and quantitative data (F) of CD63 as an exosome marker in exosomes from TGF-β1- or GW4869-treated NRK-52E cells. Numbers (1 to 3) indicate each independent treatment in the given group. * p < 0.05 versus Ctrl-Exos, # p < 0.05 versus 5 ng/ml TGFβ1-Exos, & p < 0.05 versus 15 ng/ml TGFβ1-Exos (n = 3). (G) Fluorescent staining image of PKH-67-labeled NRK-52E cells. Scales bars=50 μm. (H) Fluorescent staining image of NRK-52E cell-derived exosomes taken up by NRK-49F cells. Scales bars=10 μm. (I, K) Representative western blot (I) and quantitative data (K) of α-SMA and PCNA in NRK-49F cells incubated with exosomes from TGF-β1- or GW4869-treated NRK-52E cells. Numbers (1 to 3) indicate each independent treatment in the giving group. * p < 0.05 versus Ctrl-Exos, # p < 0.05 versus 5 ng/ml TGFβ1-Exos, & p < 0.05 versus 15 ng/ml TGFβ1-Exos (n = 3). (J) Proliferation rate of NRK-49F cells incubated with NRK-52E cell-derived exosomes measured by CCK-8. * p < 0.05 versus Ctrl-Exos, # p < 0.05 versus 5 ng/ml TGFβ1-Exos, & p < 0.05 versus 15 ng/mL TGFβ1-Exos (n = 3). (L-N) Double immunofluorescence staining (green for Col-I and red for fibronectin) demonstrates the expression of Col-I and fibronectin in NRK-49F cells incubated with NRK-52E cell-derived exosomes. Scales bars=50 μm. * p < 0.05 versus Ctrl-Exos, # p < 0.05 versus 5 ng/ml TGFβ1-Exos, & p < 0.05 versus 15 ng/mL TGFβ1-Exos.

Article Snippet: The primary antibodies were as follows: TGF-β1 (Sigma, SAB4502954), CD63 (Affinity Biosciences, AF5117), TSG-101 (Abcam, ab125011), Fibronectin (Proteintech Group, 15613-1-AP), α-SMA (Boster Biological Technology, BM0002), Collagen I (Novus Biologicals, NB600-408), E-cadherin (Abcam, ab76319), Fsp-1 (Cell Signaling Technology, 13018), PCNA (Abcam, ab92552), PTEN (Cell Signaling Technology, 9559), and p-Akt (Abcam, ab18785).

Techniques: In Vitro, Incubation, Isolation, Western Blot, Marker, Staining, Labeling, Derivative Assay, CCK-8 Assay, Double Immunofluorescence Staining, Expressing

Journal: Theranostics

Article Title: Exosomal miR-21 from tubular cells contributes to renal fibrosis by activating fibroblasts via targeting PTEN in obstructed kidneys

doi: 10.7150/thno.62820

Figure Lengend Snippet: Tubular cell-derived exosomes promote renal fibrosis in vivo . (A) Experimental design. TGFβ1-Exos or Ctrl-Exos from NRK-52E cells were injected into UUO mice by tail vein injection at 1, 3 and 5 days. (B) Representative images show the presence of PKH-67-labeled TGFβ1-Exos isolated from NRK-52E cells in mouse kidneys after intravenous injection. Kidney sections were examined at 24 h after injection. Arrows indicate PKH-67 labeled exosomes (green). Scales bars=50 μm. (C, D) Representative western blot (C) and quantitative data (D) of TSG101, CD63 and fibronectin in UUO kidneys injected with Ctrl-Exos or TGFβ1-Exos. Numbers (1 to 3) indicate each individual animal in the given group. * p < 0.05 versus sham, # p < 0.05 versus UUO7d+Ctrl-Exo (n = 6). (E, F) Representative western blot (E) and quantitative data (F) of fibronectin, Fsp-1 and PCNA in UUO kidneys injected with Ctrl-Exos or TGFβ1-Exos. Numbers (1 to 3) indicate each individual animal in the given group. * p < 0.05 versus sham, # p < 0.05 versus UUO7d+Ctrl-Exo (n = 6). (G, J) Treble immunofluorescence staining (G) and quantitative data (J) demonstrate the expression of E-cad, α-SMA and fibronectin in UUO kidneys injected with Ctrl-Exos or TGFβ1-Exos. Scales bars=50μm. * p < 0.05 versus sham, # p < 0.05 versus UUO7d+Ctrl-Exo. (H, I, K, L) Representative micrographs of Col-I immunohistochemical staining, Masson staining, Sirius red staining (H) and quantitative data (I, K, L) show fibronectin and collagen deposition in UUO kidneys injected with Ctrl-Exos or TGFβ1-Exos. Scales bars=50 μm. * p < 0.05 versus sham, # p < 0.05 versus UUO7d+Ctrl-Exo.

Article Snippet: The primary antibodies were as follows: TGF-β1 (Sigma, SAB4502954), CD63 (Affinity Biosciences, AF5117), TSG-101 (Abcam, ab125011), Fibronectin (Proteintech Group, 15613-1-AP), α-SMA (Boster Biological Technology, BM0002), Collagen I (Novus Biologicals, NB600-408), E-cadherin (Abcam, ab76319), Fsp-1 (Cell Signaling Technology, 13018), PCNA (Abcam, ab92552), PTEN (Cell Signaling Technology, 9559), and p-Akt (Abcam, ab18785).

Techniques: Derivative Assay, In Vivo, Injection, Labeling, Isolation, Western Blot, Immunofluorescence, Staining, Expressing, Immunohistochemical staining

Journal: Theranostics

Article Title: Exosomal miR-21 from tubular cells contributes to renal fibrosis by activating fibroblasts via targeting PTEN in obstructed kidneys

doi: 10.7150/thno.62820

Figure Lengend Snippet: Rab27a knockout inhibits exosome secretion and alleviates UUO-induced renal fibrosis in vivo . (A) Rab27a -/- mouse. (B, C) Rab27a knockout was confirmed by PCR screening (targeted allele: 476 bp) (B) and sequencing confirmation (C) . (D, E) Representative western blot (D) and quantitative data (E) of CD63 in Rab27a knockout kidneys after UUO (n = 6). * p < 0.05 versus sham, # p < 0.05 versus WT+UUO-7d. (F, I) Representative western blot (F) and quantitative data (I) of Fsp-1, PCNA and α-SMA in Rab27a knockout kidneys after UUO (n = 6). * p < 0.05 versus sham, # p < 0.05 versus WT+UUO-7d. (H, J) Representative immunofluorescence micrographs (J) and quantitative data (H) show Fsp-1 expression (n = 6). Scales bars=50 μm. * p < 0.05 versus sham, # p < 0.05 versus WT+UUO-7d. (G, K-M) Masson staining, Col-I immunohistochemical staining and fibronectin immunofluorescence staining indicated the deposition of collagens and fibronectin. Representative micrographs (G) and quantitative data (K-M) are presented (n = 6). Scales bars=50 μm. * p < 0.05 versus sham, # p < 0.05 versus WT+UUO-7d.

Article Snippet: The primary antibodies were as follows: TGF-β1 (Sigma, SAB4502954), CD63 (Affinity Biosciences, AF5117), TSG-101 (Abcam, ab125011), Fibronectin (Proteintech Group, 15613-1-AP), α-SMA (Boster Biological Technology, BM0002), Collagen I (Novus Biologicals, NB600-408), E-cadherin (Abcam, ab76319), Fsp-1 (Cell Signaling Technology, 13018), PCNA (Abcam, ab92552), PTEN (Cell Signaling Technology, 9559), and p-Akt (Abcam, ab18785).

Techniques: Knock-Out, In Vivo, Sequencing, Western Blot, Immunofluorescence, Expressing, Staining, Immunohistochemical staining

Journal: Theranostics

Article Title: Exosomal miR-21 from tubular cells contributes to renal fibrosis by activating fibroblasts via targeting PTEN in obstructed kidneys

doi: 10.7150/thno.62820

Figure Lengend Snippet: Tubule cell-derived exosomal miR-21 promotes fibroblast activation in vitro . (A) NRK-52E-delivered exosomal miRNA sequencing after TGF-β1 (15 ng/ml) treatment. (B) Experimental design. Concentration of TGF-β1, 15 ng/ml. (C, G-I) Representative immunofluorescence micrographs (C) and quantitative data (G-I) show Col-I, fibronectin and α-SMA expression in NRK-49F cells after stimulation with NRK-52E-delivered exosomes. Scales bars=50 μm. * p < 0.05 versus sham, # p < 0.05 versus Ctrl. (D) PCR detection of miR-21 in exosomes and NRK-52E cells after TGF-β1 treatment (n = 3). * p < 0.05 versus sham in cells, # p < 0.05 versus sham in exosomes. (E) PCR detection of miR-21 in NRK-52E-delivered exosomes after miR-21 mimic or inhibitor transfection (n = 3). * p < 0.05 versus sham, # p < 0.05 versus Ctrl. (F) Proliferation of NRK-49F cells after stimulation with exosomes from NRK-52E cells (n = 3). * p < 0.05 versus sham, # p < 0.05 versus Ctrl.

Article Snippet: The primary antibodies were as follows: TGF-β1 (Sigma, SAB4502954), CD63 (Affinity Biosciences, AF5117), TSG-101 (Abcam, ab125011), Fibronectin (Proteintech Group, 15613-1-AP), α-SMA (Boster Biological Technology, BM0002), Collagen I (Novus Biologicals, NB600-408), E-cadherin (Abcam, ab76319), Fsp-1 (Cell Signaling Technology, 13018), PCNA (Abcam, ab92552), PTEN (Cell Signaling Technology, 9559), and p-Akt (Abcam, ab18785).

Techniques: Derivative Assay, Activation Assay, In Vitro, Sequencing, Concentration Assay, Immunofluorescence, Expressing, Transfection

Journal: Theranostics

Article Title: Exosomal miR-21 from tubular cells contributes to renal fibrosis by activating fibroblasts via targeting PTEN in obstructed kidneys

doi: 10.7150/thno.62820

Figure Lengend Snippet: Tubule cell-derived exosomal miR-21 mediates fibroblast activation through the PTEN/AKT pathway in vitro . (A) Experimental design. Concentration of TGF-β1, 15 ng/ml. (B) PTEN mRNA level after siPTEN treatment. NS, no significant difference versus Ctrl, # p < 0.05 versus Ctrl. (C) Proliferation of NRK-49F cells after miR-21 inhibitor or siPTEN transfection (n = 3). # p < 0.05. (D-G) Representative immunofluorescence micrographs (G) and quantitative data (D-F) show Col-I, fibronectin and α-SMA expression in NRK-49F cells after miR-21 inhibitor or siPTEN transfection (n = 3). Scales bars=50 μm. # p < 0.05. (H-K) Representative western blot (H) and quantitative data (I-K) show PTEN, Akt, p-Akt and PCNA expression in NRK-49F cells after miR-21 inhibitor or siPTEN transfection (n = 3). # p < 0.05.

Article Snippet: The primary antibodies were as follows: TGF-β1 (Sigma, SAB4502954), CD63 (Affinity Biosciences, AF5117), TSG-101 (Abcam, ab125011), Fibronectin (Proteintech Group, 15613-1-AP), α-SMA (Boster Biological Technology, BM0002), Collagen I (Novus Biologicals, NB600-408), E-cadherin (Abcam, ab76319), Fsp-1 (Cell Signaling Technology, 13018), PCNA (Abcam, ab92552), PTEN (Cell Signaling Technology, 9559), and p-Akt (Abcam, ab18785).

Techniques: Derivative Assay, Activation Assay, In Vitro, Concentration Assay, Transfection, Immunofluorescence, Expressing, Western Blot

Journal: Theranostics

Article Title: Exosomal miR-21 from tubular cells contributes to renal fibrosis by activating fibroblasts via targeting PTEN in obstructed kidneys

doi: 10.7150/thno.62820

Figure Lengend Snippet: Tubular cell-derived exosomal miR-21 promotes renal fibrosis through the PTEN/AKT pathway in vivo . (A-D) Representative immunofluorescence micrographs (A) and quantitative data (B-D) show Col-I, fibronectin and α-SMA expression in mouse kidneys after intravenous exosome injection (n = 6). Scales bars=50 μm. * p < 0.05 versus Ctrl-Exo, # p < 0.05 versus TGFβ1-Exo. (E-I) Representative western blot (F) and quantitative data (E, G-I) show Fsp-1, PCNA, PTEN, Akt and p-Akt expression in mouse kidneys after intravenous exosome injection (n = 6). * p < 0.05 versus Ctrl-Exo, # p < 0.05 versus TGFβ1-Exo.

Article Snippet: The primary antibodies were as follows: TGF-β1 (Sigma, SAB4502954), CD63 (Affinity Biosciences, AF5117), TSG-101 (Abcam, ab125011), Fibronectin (Proteintech Group, 15613-1-AP), α-SMA (Boster Biological Technology, BM0002), Collagen I (Novus Biologicals, NB600-408), E-cadherin (Abcam, ab76319), Fsp-1 (Cell Signaling Technology, 13018), PCNA (Abcam, ab92552), PTEN (Cell Signaling Technology, 9559), and p-Akt (Abcam, ab18785).

Techniques: Derivative Assay, In Vivo, Immunofluorescence, Expressing, Injection, Western Blot

Journal: Journal of Molecular Cell Biology

Article Title: CCT6A alleviates pulmonary fibrosis by inhibiting HIF-1α-mediated lactate production

doi: 10.1093/jmcb/mjae021

Figure Lengend Snippet: Activation of lactate signal promotes pulmonary fibrosis in mice. ( A ) Timeline of GPR81 agonist-treated mouse lung fibrosis model. ( B ) Quantification of hydroxyproline content in mouse right inferior lobe ( n = 4 mice per group). ( C ) Quantification of total cells in BALF ( n = 3). ( D ) Protein concentration in BALF ( n = 3). ( E ) Representative images of H&E and Masson's Trichrome staining in mouse lung sections ( n = 3). Scale bar, 50 μm. The Ashcroft score was determined to indicate the severity of fibrosis. ( F ) Western blotting and quantification of fibrosis marker expression in whole lung lysates ( n = 3). ( G and H ) qPCR analysis of α-SMA, Col1a1, and Fn1 mRNA expression levels and immunofluorescence staining of lipid droplet in mouse lung tissue samples ( n = 4). Scale bar, 50 μm. * P < 0.05, ** P <0.01, *** P < 0.001, **** P <0.0001.

Article Snippet: FN1 , Polyclonal rabbit , Proteintech, 15613-1-AP , 1:2000.

Techniques: Activation Assay, Protein Concentration, Staining, Western Blot, Marker, Expressing, Immunofluorescence

Journal: Journal of Molecular Cell Biology

Article Title: CCT6A alleviates pulmonary fibrosis by inhibiting HIF-1α-mediated lactate production

doi: 10.1093/jmcb/mjae021

Figure Lengend Snippet: Cct6a restores BLM-induced lung fibrosis in mice. ( A ) Timeline of AAV-treated mouse lung fibrosis model. ( B ) Hydroxyproline in the right inferior lobe (Vehicle Sal n = 7, Cct6a Sal n = 8, Vehicle BLM n = 8, Cct6a BLM n = 7). ( C ) Total cell counts in BALF ( n = 7 mice per group). ( D ) Protein concentration in BALF (Vehicle Sal n = 7, Cct6a Sal n = 7, Vehicle BLM n = 8, Cct6a BLM n = 9). ( E ) Representative images of micro CT scans of mouse lung density ( n = 3). ( F ) Representative images of H&E and Masson's Trichrome staining in mouse lung sections ( n = 3). Boxed regions in the right superior panel are panoramic images of the lung tissue sections. Scale bar, 50 μm. The Ashcroft score was determined to indicate the severity of fibrosis. ( G ) Lactate level in mouse serum (Vehicle Sal n = 8, Cct6a Sal n = 10, Vehicle BLM n = 9, Cct6a BLM n = 10). ( H ) Western blotting and quantification of fibrosis marker expression in whole lung lysates ( n = 3). ( I ) qPCR analysis of Col1a1, Col3a1, Fn1, and Ctgf mRNA expression levels in the lung homogenate ( n = 6). ( J ) Immunoblot analysis of Vhl, Hif-1α, and Ldha protein levels in whole lung lysates ( n = 3). ( K ) Immunofluorescence staining of lipid droplet in mouse lung sections ( n = 3). Scale bar, 50 μm. * P < 0.05, ** P <0.01, *** P < 0.001, **** P <0.0001.

Article Snippet: FN1 , Polyclonal rabbit , Proteintech, 15613-1-AP , 1:2000.

Techniques: Protein Concentration, Micro-CT, Staining, Western Blot, Marker, Expressing, Immunofluorescence

Journal: Journal of Molecular Cell Biology

Article Title: CCT6A alleviates pulmonary fibrosis by inhibiting HIF-1α-mediated lactate production

doi: 10.1093/jmcb/mjae021

Figure Lengend Snippet: Primers and oligonucleotides.

Article Snippet: FN1 , Polyclonal rabbit , Proteintech, 15613-1-AP , 1:2000.

Techniques:

Journal: Journal of Molecular Cell Biology

Article Title: CCT6A alleviates pulmonary fibrosis by inhibiting HIF-1α-mediated lactate production

doi: 10.1093/jmcb/mjae021

Figure Lengend Snippet: List of antibodies used in this study.

Article Snippet: FN1 , Polyclonal rabbit , Proteintech, 15613-1-AP , 1:2000.

Techniques: Ubiquitin Proteomics