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ATCC human cell lines mrc5
Human Cell Lines Mrc5, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 5494 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/mrc5+cell+lines/MRC-5/10__3390_slash_microbiolres17060105-126-7-15
Average 99 stars, based on 5494 article reviews

human cell lines mrc5 - by Bioz Stars, 2026-11

99/100 stars

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Article Title: A bispecific nanobody-drug conjugate targeting TROP2 and c-Met for low-concentration, single-dose treatment of pancreatic cancer.
Article Snippet: REAGENT or RESOURCE SOURCE IDENTIFIER Phalloidin Labeling Probes Thermo Fisher Scientific Cat#A12379 PageRuler TM Prestained Protein Ladder Thermo Fisher Scientific Cat#26616 Sacituzumab govitecan MedChemExpress (MCE) HY-132254; CAS No.1491917-83-9 Telisotuzumab vedotin MedChemExpress (MCE) HY-141601; CAS No.1714088-51-3 Cathepsin B Protein, Human (His) MedChemExpress (MCE) Cat#HY-P70830 TROP2 Protein, Human, Recombinant (His Tag) Sinobiological Cat#10428-H08H c-MET Protein, Human, Recombinant (ECD, His Tag) Sinobiological Cat#10692-H08H Critical commercial assays Opal 7-color Manual IHC Kit BIOMART.CN Cat#NEL811001KT Cell Cycle and Apoptosis Analysis Kit BEYOTIME Cat#C1052 Annexin V-FITC/PI Apoptosis Detection Kit BEYOTIME Cat#C1063 Cell Counting Kit-8 MedChemExpress (MCE) Cat#HY-K0301 Sensor Chip Protein A Cytiva Cat#10349316 Deposited data TROP2 protein structure This paper PDB: 7PEE c-Met protein structure This paper PDB: 2UZX TROP2 and c-Met expression profiles in patients with tumors versus healthy controls HPA (The Human Protein Atlas) HPA:https://www.proteinatlas.org/search/ tacstd2,; https://www.proteinatlas.org/ search/MET TROP2 and MET expression and survival in Cancers GEPIA2 http://gepia2.cancer-pku.cn/ GEPIA:http:// gepia.cancer-pku.cn/ detail.php?gene=TACSTD2; http:// gepia.cancer-pku.cn/ detail.php?gene=MET Experimental models: Cell lines BxPC-3 ATCC CRL-1687 TM NCI-H358 ATCC CRL-5807 TM SPC-A1 This paper N/A MDA-MB-231 ATCC HTB-26 TM HT-29 ATCC HTB-38 TM OVCAR3 ATCC HTB-161 TM SW1990 ATCC CRL-2172 TM HPAC ATCC CRL-2119 TM PANC02.03 ATCC CRL-2553 TM Capan-2 ATCC HTB-80 TM ASPC1 ATCC CRL-1682 TM HCT-116 ATCC CCL-247 TM HCC94 This paper N/A HUVEC ScienCell Cat#8000 MRC-5 ATCC CCL-171 TM 293T ATCC CRL-3216 TM HEK293 ATCC CRL-1573 TM Experimental models: Organisms/strains Mouse: BALB/cNj-Foxn1nu/Gpt GemPharmatech Cat#D000521 Mouse: NOD.Cg-PrkdcscidIl2rgem1Smoc Shanghai Model Organisms Cat#NM-NSG-001 Mouse: C57BL/6-Tacstd2tm1(TACSTD2) Bcgen/Bcgen Biocytogen Cat#110966 (Continued on next page) e2 Cell Reports Medicine 7, 102688, April 21, 2026 OPEN ACCESS .. The BxPC-3, NCI-H358, SPC-A1, MDA-MB-231, HT-29, OVCAR3, SW1990, HPAC, PANC02.03, Capan-2, ASPC1, HCT-116, HCC94, HUVEC and MRC5 cell lines were obtained from the American Type Culture Collection (ATCC; Manassas, VA, USA). .. Expi293F cells were obtained from Thermo Fisher Scientific (Gibco, USA).

Article Title: A bispecific nanobody-drug conjugate targeting TROP2 and c-Met for low-concentration, single-dose treatment of pancreatic cancer
Article Snippet: .. The BxPC-3, NCI-H358, SPC-A1, MDA-MB-231, HT-29, OVCAR3, SW1990, HPAC, PANC02.03, Capan-2, ASPC1, HCT-116, HCC94, HUVEC and MRC5 cell lines were obtained from the American Type Culture Collection (ATCC; Manassas, VA, USA). .. Expi293F cells were obtained from Thermo Fisher Scientific (Gibco, USA).

Cell Culture:

Article Title: 1,2,3-triazole and chiral Schiff base hybrids as potential anticancer agents: DFT, molecular docking and ADME studies
Article Snippet: .. PC3, A375, and MRC5 cell lines were purchased from ATCC and were cultured in Dulbecco’s Modified Eagle Media (DMEM) supplemented with 10% Fetal Bovine Serum (FBS) (Highveld biological), 1% gentamycin and 1% penicillin/streptomycin (Sigma, USA). ..

Article Title: Drug resistant pancreatic cancer cells exhibit altered biophysical interactions with stromal fibroblasts in imaging studies of 3D co-culture models
Article Snippet: .. PANC1 and MRC5 cell lines were acquired from ATCC and maintained in T75 cell culture flasks according to ATCC guidelines. .. DMEM and MEM (HyClone) were supplemented with 10% FBS (HyClone), 100 IU/mL penicillin, 1% streptomycin (HyClone), and 0.5 mg/mL amphotericin B (Corning).

Article Title: Drug resistant pancreatic cancer cells exhibit altered biophysical interactions with stromal fibroblasts in imaging studies of 3D co-culture models
Article Snippet: .. PANC1 and MRC5 cell lines were acquired from ATCC and maintained in T75 cell culture flasks according to ATCC guidelines. .. DMEM and MEM (HyClone) were supplemented with 10% FBS (HyClone), 100IU/mL penicillin, 1% streptomycin (HyClone), and 0.5 mg/mL amphotericin B (Corning).

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Article Title: One-pot synthesis of novel poly-substituted 3-cyanopyridines: Molecular docking, antimicrobial, cytotoxicity, and DFT/TD-DFT studies
Article Snippet: Novel pyridine-3-carbonitrile derivatives, denoted as (4a-j), were synthesized using a convergent synthetic approach that involved a one-pot four-component reaction.. This was achieved by utilizing a combination of various aromatic aldehydes, acetophenone derivatives, malononitrile, and four different sodium alkoxide solutions.. The synthesized compounds were characterized using various spectroscopic techniques such as IR, 1HNMR , 13CNMR , and elemental analysis.

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TRIM36 inhibits lung fibroblast proliferation, migration, and differentiation (A) The efficiency of TRIM36 overexpression was detected by immunoblotting. (B and C) Cell proliferation assessed by CCK-8 assay in MRC5 and IMR-90 cells transfected with indicated plasmids ( n = 3). (D and E) Cell proliferation evaluated by EdU assay in MRC5 and IMR-90 cells transfected with indicated plasmids ( n = 3). Positive cell numbers are quantified in bar graphs. Scale bars: 100 μm. (F and G) Cell migration evaluated by Transwell assay in MRC5 and IMR-90 cells transfected with indicated plasmids ( n = 3). Migrated cell numbers are quantified in bar graphs. Scale bars: 100 μm. (H and I) MRC5 and IMR-90 cells were transfected with the indicated plasmids and treated with dimethyl sulfoxide (DMSO) or TGF-β1 (10 ng/mL) for 24 h before lysis. Immunoblot analysis was performed using indicated antibodies. (J and K) The expression intensity of Fibronectin 1, Collagen 1, and α-SMA in (H) and (I) were quantified by densitometry, with GAPDH as a normalizer. Each data point represents the test result of one sample. The lanes in western blots correspond to technical replicates, and similar results were repeated in three biologically independent experiments. Data are shown as the means ± SD. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001.

Journal: iScience

Article Title: TRIM36 inhibits lung fibroblast activation and pulmonary fibrosis through the degradation of phospho-AKT1

doi: 10.1016/j.isci.2025.113775

Figure Lengend Snippet: TRIM36 inhibits lung fibroblast proliferation, migration, and differentiation (A) The efficiency of TRIM36 overexpression was detected by immunoblotting. (B and C) Cell proliferation assessed by CCK-8 assay in MRC5 and IMR-90 cells transfected with indicated plasmids ( n = 3). (D and E) Cell proliferation evaluated by EdU assay in MRC5 and IMR-90 cells transfected with indicated plasmids ( n = 3). Positive cell numbers are quantified in bar graphs. Scale bars: 100 μm. (F and G) Cell migration evaluated by Transwell assay in MRC5 and IMR-90 cells transfected with indicated plasmids ( n = 3). Migrated cell numbers are quantified in bar graphs. Scale bars: 100 μm. (H and I) MRC5 and IMR-90 cells were transfected with the indicated plasmids and treated with dimethyl sulfoxide (DMSO) or TGF-β1 (10 ng/mL) for 24 h before lysis. Immunoblot analysis was performed using indicated antibodies. (J and K) The expression intensity of Fibronectin 1, Collagen 1, and α-SMA in (H) and (I) were quantified by densitometry, with GAPDH as a normalizer. Each data point represents the test result of one sample. The lanes in western blots correspond to technical replicates, and similar results were repeated in three biologically independent experiments. Data are shown as the means ± SD. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001.

Article Snippet: Human cell line: MRC5 , ATCC , Cat# CCL-171.

Techniques: Migration, Over Expression, Western Blot, CCK-8 Assay, Transfection, EdU Assay, Transwell Assay, Lysis, Expressing

TRIM36 destabilizes AKT1 (A) Endogenous interaction between TRIM36 and AKT1. MRC5 and IMR-90 cells were collected and lysed. The extracts were IP using indicated antibodies. (B and C) Schematic diagram indicated the structure of TRIM36 (B) and AKT1 (C) and their deletion mutants. FLAG-TRIM36 WT or deletion mutants were co-transfected with HA-AKT1 in human embryonic kidney 293T (HEK293T) cells (B). FLAG-AKT1 WT or deletion mutants were co-transfected with HA-TRIM36 in HEK293T cells (C). HEK293T cells were collected and lysed. IP was performed using anti-FLAG magnetic beads and analyzed by immunoblotting. (D) TRIM36 shorten AKT1 protein half-life. Cells ectopically expressing TRIM36 were treated with CHX (100 μg/mL) for indicated times. The cells were collected and analyzed by immunoblotting with the indicated antibodies. (E) The expression intensities of AKT1, p-AKT1(T308), and p-AKT1(S473) at each time point in (D) were quantified by densitometry, with GAPDH as a normalizer. (F) TRIM36 overexpression cells were treated with TGF-β1 (10 ng/mL). The cells were collected and analyzed by immunoblotting with the indicated antibodies. Similar results were repeated in three biologically independent experiments. Data are shown as the means ± SD. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001.

Journal: iScience

Article Title: TRIM36 inhibits lung fibroblast activation and pulmonary fibrosis through the degradation of phospho-AKT1

doi: 10.1016/j.isci.2025.113775

Figure Lengend Snippet: TRIM36 destabilizes AKT1 (A) Endogenous interaction between TRIM36 and AKT1. MRC5 and IMR-90 cells were collected and lysed. The extracts were IP using indicated antibodies. (B and C) Schematic diagram indicated the structure of TRIM36 (B) and AKT1 (C) and their deletion mutants. FLAG-TRIM36 WT or deletion mutants were co-transfected with HA-AKT1 in human embryonic kidney 293T (HEK293T) cells (B). FLAG-AKT1 WT or deletion mutants were co-transfected with HA-TRIM36 in HEK293T cells (C). HEK293T cells were collected and lysed. IP was performed using anti-FLAG magnetic beads and analyzed by immunoblotting. (D) TRIM36 shorten AKT1 protein half-life. Cells ectopically expressing TRIM36 were treated with CHX (100 μg/mL) for indicated times. The cells were collected and analyzed by immunoblotting with the indicated antibodies. (E) The expression intensities of AKT1, p-AKT1(T308), and p-AKT1(S473) at each time point in (D) were quantified by densitometry, with GAPDH as a normalizer. (F) TRIM36 overexpression cells were treated with TGF-β1 (10 ng/mL). The cells were collected and analyzed by immunoblotting with the indicated antibodies. Similar results were repeated in three biologically independent experiments. Data are shown as the means ± SD. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001.

Article Snippet: Human cell line: MRC5 , ATCC , Cat# CCL-171.

Techniques: Transfection, Magnetic Beads, Western Blot, Expressing, Over Expression

TRIM36 promotes proteasomal degradation of AKT1 via K48-linked ubiquitination at lysine 268 (A) MRC5 and IMR-90 cells ectopically expressing TRIM36 were treated with MG132 or DMSO for 5 h. Cells were collected and analyzed by immunoblotting with the indicated antibodies. (B and C) HEK293T cells were transfected with the indicated plasmids and treated with MG132 for 5 h. The cells were collected and lysed in RIPA buffer. Immunoprecipitated AKT1 was analyzed by immunoblotting with the indicated antibodies. (D) The polyubiquitination of AKT1 in the presence of TRIM36 and either WT ubiquitin or its mutants. HEK293T cells were transfected with the indicated plasmids. 48 h after transfection, cells were treated with MG132 for 5 h before lysis. IP and immunoblot analysis were performed as described in (B). (E) The K268 sites of AKT1 are highly conserved across species. (F) The polyubiquitination of AKT1 WT and its mutants. HEK293T cells were transfected with the indicated plasmids. IP and immunoblot analysis were performed as described in (B). Similar results were repeated in three biologically independent experiments.

Journal: iScience

Article Title: TRIM36 inhibits lung fibroblast activation and pulmonary fibrosis through the degradation of phospho-AKT1

doi: 10.1016/j.isci.2025.113775

Figure Lengend Snippet: TRIM36 promotes proteasomal degradation of AKT1 via K48-linked ubiquitination at lysine 268 (A) MRC5 and IMR-90 cells ectopically expressing TRIM36 were treated with MG132 or DMSO for 5 h. Cells were collected and analyzed by immunoblotting with the indicated antibodies. (B and C) HEK293T cells were transfected with the indicated plasmids and treated with MG132 for 5 h. The cells were collected and lysed in RIPA buffer. Immunoprecipitated AKT1 was analyzed by immunoblotting with the indicated antibodies. (D) The polyubiquitination of AKT1 in the presence of TRIM36 and either WT ubiquitin or its mutants. HEK293T cells were transfected with the indicated plasmids. 48 h after transfection, cells were treated with MG132 for 5 h before lysis. IP and immunoblot analysis were performed as described in (B). (E) The K268 sites of AKT1 are highly conserved across species. (F) The polyubiquitination of AKT1 WT and its mutants. HEK293T cells were transfected with the indicated plasmids. IP and immunoblot analysis were performed as described in (B). Similar results were repeated in three biologically independent experiments.

Article Snippet: Human cell line: MRC5 , ATCC , Cat# CCL-171.

Techniques: Ubiquitin Proteomics, Expressing, Western Blot, Transfection, Immunoprecipitation, Lysis

TRIM36 preferentially ubiquitinates the phospho-AKT1 (T308/S473) (A) HEK293T cells were transfected with FLAG-TRIM36 and HA-AKT1 plasmids for 48 h. The cells lysates were treated with λ protein phosphatase for 30 min, followed by IP using anti-FLAG magnetic beads and immunoblot analysis. (B and C) HEK293T cells were transfected with the indicated plasmids and treated with 2 μM MK2206 or 4 μg/mL SC79. IP and immunoblot analysis were performed as described in (A). (D) HEK293T cells were transfected with vectors expressing HA-AKT1 WT or its mutants and progressive increasing doses of Myc-TRIM36. Cells were collected and analyzed by immunoblotting with the indicated antibodies. (E) The polyubiquitination of AKT1 WT or its mutants. HEK293T cells were transfected with indicated plasmids and treated with MG132 for 5 h before lysis. IP and immunoblot analysis were performed as described in ( B). (F) Interaction between TRIM36 and AKT1 WT or its mutants. HEK293T cells were transfected with indicated plasmids. IP and immunoblot analysis were performed as described in (A). (G) Glutathione S-transferase (GST) pull-down assays indicated the interaction between GST-TRIM36 and His-AKT1 WT or its mutants. (H) Endogenous interaction between TRIM36 and phospho-AKT1 (S473). MRC5 and IMR-90 cells were collected and lysed. The extracts were IP using phospho-AKT1 (S473) antibody. Immunoblot analysis was performed as described in (A). Similar results were repeated in three biologically independent experiments.

Journal: iScience

Article Title: TRIM36 inhibits lung fibroblast activation and pulmonary fibrosis through the degradation of phospho-AKT1

doi: 10.1016/j.isci.2025.113775

Figure Lengend Snippet: TRIM36 preferentially ubiquitinates the phospho-AKT1 (T308/S473) (A) HEK293T cells were transfected with FLAG-TRIM36 and HA-AKT1 plasmids for 48 h. The cells lysates were treated with λ protein phosphatase for 30 min, followed by IP using anti-FLAG magnetic beads and immunoblot analysis. (B and C) HEK293T cells were transfected with the indicated plasmids and treated with 2 μM MK2206 or 4 μg/mL SC79. IP and immunoblot analysis were performed as described in (A). (D) HEK293T cells were transfected with vectors expressing HA-AKT1 WT or its mutants and progressive increasing doses of Myc-TRIM36. Cells were collected and analyzed by immunoblotting with the indicated antibodies. (E) The polyubiquitination of AKT1 WT or its mutants. HEK293T cells were transfected with indicated plasmids and treated with MG132 for 5 h before lysis. IP and immunoblot analysis were performed as described in ( B). (F) Interaction between TRIM36 and AKT1 WT or its mutants. HEK293T cells were transfected with indicated plasmids. IP and immunoblot analysis were performed as described in (A). (G) Glutathione S-transferase (GST) pull-down assays indicated the interaction between GST-TRIM36 and His-AKT1 WT or its mutants. (H) Endogenous interaction between TRIM36 and phospho-AKT1 (S473). MRC5 and IMR-90 cells were collected and lysed. The extracts were IP using phospho-AKT1 (S473) antibody. Immunoblot analysis was performed as described in (A). Similar results were repeated in three biologically independent experiments.

Article Snippet: Human cell line: MRC5 , ATCC , Cat# CCL-171.

Techniques: Transfection, Magnetic Beads, Western Blot, Expressing, Lysis

TRIM36 inhibits lung fibroblast activation by suppressing AKT1 activity (A) MRC5 cells were transfected with the indicated plasmids and treated with DMSO or MK2206 for 24 h before lysis. Immunoblot analysis was performed using indicated antibodies. (B–E) Edu and Transwell assays were performed in the cells from (A). Positive cell numbers of (B) are quantified in bar graphs. The cell number of (D) was counted and exhibited in the bar graphs. n = 3. Scale bars: 100 μm. (F) MRC5 cells were transfected with TRIM36 and AKT WT or its mutants. Immunoblot analysis was performed using the indicated antibodies. (G–J) Edu and Transwell assays were performed in the cells from (F). Positive cell numbers of (G) are quantified in bar graphs. The cell number of (I) was counted and exhibited in the bar graphs. n = 3. Scale bars: 100 μm. Each data point represents the test result of one sample. (A and F) Three biological replicates (BioRep). Data are shown as the means ± SD. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001.

Journal: iScience

Article Title: TRIM36 inhibits lung fibroblast activation and pulmonary fibrosis through the degradation of phospho-AKT1

doi: 10.1016/j.isci.2025.113775

Figure Lengend Snippet: TRIM36 inhibits lung fibroblast activation by suppressing AKT1 activity (A) MRC5 cells were transfected with the indicated plasmids and treated with DMSO or MK2206 for 24 h before lysis. Immunoblot analysis was performed using indicated antibodies. (B–E) Edu and Transwell assays were performed in the cells from (A). Positive cell numbers of (B) are quantified in bar graphs. The cell number of (D) was counted and exhibited in the bar graphs. n = 3. Scale bars: 100 μm. (F) MRC5 cells were transfected with TRIM36 and AKT WT or its mutants. Immunoblot analysis was performed using the indicated antibodies. (G–J) Edu and Transwell assays were performed in the cells from (F). Positive cell numbers of (G) are quantified in bar graphs. The cell number of (I) was counted and exhibited in the bar graphs. n = 3. Scale bars: 100 μm. Each data point represents the test result of one sample. (A and F) Three biological replicates (BioRep). Data are shown as the means ± SD. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001.

Article Snippet: Human cell line: MRC5 , ATCC , Cat# CCL-171.

Techniques: Activation Assay, Activity Assay, Transfection, Lysis, Western Blot

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