ATCC
enterococcus mundtii atcc 43186 Enterococcus Mundtii Atcc 43186, supplied by ATCC, 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/result/enterococcus mundtii atcc 43186/product/ATCC Average 94 stars, based on 1 article reviews
enterococcus mundtii atcc 43186 - by Bioz Stars,
2025-06
94/100 stars
|
Buy from Supplier |
Santa Cruz Biotechnology
tenascin c ![]() Tenascin C, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more https://www.bioz.com/result/tenascin c/product/Santa Cruz Biotechnology Average 85 stars, based on 1 article reviews
tenascin c - by Bioz Stars,
2025-06
85/100 stars
|
Buy from Supplier |
Santa Cruz Biotechnology
tnc shrna lentiviral particle ![]() Tnc Shrna Lentiviral Particle, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 88/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more https://www.bioz.com/result/tnc shrna lentiviral particle/product/Santa Cruz Biotechnology Average 88 stars, based on 1 article reviews
tnc shrna lentiviral particle - by Bioz Stars,
2025-06
88/100 stars
|
Buy from Supplier |
Santa Cruz Biotechnology
tnc shrna lentiviral particles ![]() Tnc Shrna Lentiviral Particles, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 88/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more https://www.bioz.com/result/tnc shrna lentiviral particles/product/Santa Cruz Biotechnology Average 88 stars, based on 1 article reviews
tnc shrna lentiviral particles - by Bioz Stars,
2025-06
88/100 stars
|
Buy from Supplier |
DSMZ
strain a flexuosa dsm43186 ![]() Strain A Flexuosa Dsm43186, supplied by DSMZ, used in various techniques. Bioz Stars score: 85/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more https://www.bioz.com/result/strain a flexuosa dsm43186/product/DSMZ Average 85 stars, based on 1 article reviews
strain a flexuosa dsm43186 - by Bioz Stars,
2025-06
85/100 stars
|
Buy from Supplier |
Image Search Results

Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
Article Title: Arterial Wall Stress Controls NFAT5 Activity in Vascular Smooth Muscle Cells
doi: 10.1161/JAHA.113.000626
Figure Lengend Snippet: Transcriptional targets of NFAT5 upon biomechanical stretch. Volcano plot analysis of transcriptome changes (fold expression level vs calculated probability value) in HUASMCs transfected with control or NFAT5 siRNA shows nearly 2000 differently regulated genes for P <0.005 (A, n=3 for all experimental groups). Verification of 4 microarray targets by RT‐PCR (B, ** P <0.01, *** P <0.001 vs control, n=3 for all experimental groups). There are 7 putative NFAT5 binding sites in the human tenascin‐C promotor as evidenced by in silico analysis of the first 3512 bp of the promoter sequence upstream of the transcription start site. C, The maximum core similarity (core similarity of 1.0) is only reached when the highest conserved bases of a matrix are exactly matched by the sequence (cf. capitals in the sequence). A good match to the matrix has a similarity of >0.80 (matrix similarity). Based on a ChIP DNA fragment length in the range of 500 to 800 bp the primer pair used for ChIP analysis (651 to 807 bp) focuses on the NFAT5 binding site no. 1 (819 to 837 bp). Exemplary ChIP analysis functionally verified the stretch‐induced binding of NFAT5 to this site (D, ChIP DNA panel). Total input DNA serves as a control to verify that almost equal DNA amounts were used for the analysis. The no‐antibody‐control (NAC) reveales all non‐specifically precipitated chromatin species, the IgG control unspecific antibody binding. ACTBL2 indicates actin, beta‐like 2; ChIP, chromatin immune‐precipitation; HUASMCs, human arterial smooth muscle cells; JAM3, junctional adhesion molecule 3; NFAT5, nuclear factor of activated T‐cells; RARB, retinoic acid receptor beta; TNC, tenascin‐C.
Article Snippet: HUASMCs were transfected with short interfering RNA directed against NFAT5 (5′‐ CCA GTT CCT ACA ATG ATA A ‐3′),
Techniques: Expressing, Transfection, Microarray, Reverse Transcription Polymerase Chain Reaction, Binding Assay, In Silico, Sequencing

Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
Article Title: Arterial Wall Stress Controls NFAT5 Activity in Vascular Smooth Muscle Cells
doi: 10.1161/JAHA.113.000626
Figure Lengend Snippet: Transcriptional Targets of NFAT5 in Stretch‐Stimulated HUASMCs
Article Snippet: HUASMCs were transfected with short interfering RNA directed against NFAT5 (5′‐ CCA GTT CCT ACA ATG ATA A ‐3′),
Techniques: Expressing, Histone Deacetylase Assay, Sequencing, Binding Assay

Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
Article Title: Arterial Wall Stress Controls NFAT5 Activity in Vascular Smooth Muscle Cells
doi: 10.1161/JAHA.113.000626
Figure Lengend Snippet: Attenuation of TNC mRNA expression in stretch‐stimulated HUASMCs upon NFAT5‐dODN treatment. HUASMCs were pretreated (10 μmol/L) with control deoxyoligonucleotides (ODNscr; ODNscrFor: 5′GAGTGAAGGCATACTGACTC′3, ODNscrRev: 5′GAGTCAGTATGCCTTCACTC′3; 5′/3′‐ends were modified by phosphorothioate) or decoy oligo‐deoxynucleotides mimicking the NFAT5 binding site (NFAT5‐dODN, NFAT5‐dODNFor: 5′GAGTGGAAACATACTGACTC′3; NFAT5‐dODNRev: 5′GAGTCAGTATGTTTCCACTC′3; 5′/3′‐ends were modified by phosphorothioate) for 3 hours and exposed to biomechanical stretch for 24 hours (0.5 Hz, 0% to 13% elongation). Subsequent PCR analyses revealed that the stretch‐induced increase of tenascin C (TNC) mRNA expression is significantly attenuated in HUASMCs treated with the NFAT5‐dODN (* P <0.05 vs stretch+ODNscr and stretch, 1 out of 2 independent experiments with similar results performed in quadruplicates). HUASMCs indicates human arterial smooth muscle cells; NFAT5, nuclear factor of activated T‐cells; PCR, polymerase chain reaction; RPL32, ribosomal protein L3.
Article Snippet: HUASMCs were transfected with short interfering RNA directed against NFAT5 (5′‐ CCA GTT CCT ACA ATG ATA A ‐3′),
Techniques: Expressing, Modification, Binding Assay, Polymerase Chain Reaction

Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
Article Title: Arterial Wall Stress Controls NFAT5 Activity in Vascular Smooth Muscle Cells
doi: 10.1161/JAHA.113.000626
Figure Lengend Snippet: Inhibition of JNK blocks stretch‐induced RARB and TNC expression. HUASMCs were exposed to biomechanical stretch for 24 hours, treated with DMSO (control) or the JNK inhibitor SP600125 and the mRNA expression of the NFAT5 target genes RARB and tenascin C (TNC) was determined by real time PCR. Stretch up‐regulates RARB and TNC mRNA expression (A and B: * P <0.05 vs DMSO, n=3), which is inhibited upon SP600125 treatment (A and B: # P <0.05 vs stretch+DMSO, n=3). HUASMCs indicates human arterial smooth muscle cells; JNK, c‐Jun‐N‐terminal kinase; NFAT5, nuclear factor of activated T‐cells; PCR, polymerase chain reaction; RARB, retinoic acid receptor beta; RPL32, ribosomal protein L3.
Article Snippet: HUASMCs were transfected with short interfering RNA directed against NFAT5 (5′‐ CCA GTT CCT ACA ATG ATA A ‐3′),
Techniques: Inhibition, Expressing, Real-time Polymerase Chain Reaction, Polymerase Chain Reaction

Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
Article Title: Arterial Wall Stress Controls NFAT5 Activity in Vascular Smooth Muscle Cells
doi: 10.1161/JAHA.113.000626
Figure Lengend Snippet: Dynamics of NFAT5 expression/translocation and TNC expression in stretch‐stimulated HUASMCs. Cells were exposed to biomechanical stretch for 6, 24, and 48 hours (0.5 Hz, 0% to 13% elongation). Western blot analyses of nuclear protein fractions (H‐H3: histone H3) and cytoplasmic protein fractions (A) as well as detection of NFAT5‐specific immunofluorescence in the nuclei (B) reveal a robust nuclear localization of NFAT5 24 hours upon onset of stretch stimulation (A, * P <0.05 vs control; n.s.—not significant vs control; A, n=3 for all experimental groups (repeated measures ANOVA); B, n.s.—not significant vs control, * P <0.05 vs control with n=5 for control, n=3 for 6 hours, n=6 for 24 hours and n=3 for 48 hours). Tenascin‐C (TNC) mRNA expression is significantly increased in HUASMC exposed to stretch for 24 but not 6 hours (C, n.s.—not significant vs control, * P <0.05 vs control, with n=5 for control, n=3 for 6 hours, n=3 for 24 hours, and n=3 for 48 hours; TNC expression was normalized to RPL32 expression). HUASMCs indicates human arterial smooth muscle cells; RPL32, ribosomal protein L3.
Article Snippet: HUASMCs were transfected with short interfering RNA directed against NFAT5 (5′‐ CCA GTT CCT ACA ATG ATA A ‐3′),
Techniques: Expressing, Translocation Assay, Western Blot, Immunofluorescence

Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
Article Title: Arterial Wall Stress Controls NFAT5 Activity in Vascular Smooth Muscle Cells
doi: 10.1161/JAHA.113.000626
Figure Lengend Snippet: Tenascin‐C promotes and partially rescues HUASMC migration upon loss of NFAT5. Cells were stretched for 24 hours and tenascin‐C (TNC) mRNA expression was compared to that of static control cells (A) (* P <0.05 vs control, n=3 for all experimental groups). Spheroid sprouting assay of control and HUASMCs exposed to recombinant human tenascin‐C demonstrates a stimulating effect of tenascin‐C (TNC) on both cell migration and invasion (B through D, ** P <0.01 vs control, n=5 for all experimental groups, scale bar: 100 μm). siRNA‐mediated knockdown of TNC inhibits migration (48 hours) of HUASMCs (E through G, * P <0.05 vs ctr. siRNA, n=5 for all experimental groups). In contrast to control siRNA‐treated HUASMCs, planar migration is inhibited upon NFAT5 silencing as evidenced by quantifying their migration distance 24 and 48 hours after initiating the assay. This is partially rescued by coating the migration surface with recombinant TNC (0.65 μg/cm² rhTNC) (H, *** P <0.001/** P <0.01 vs control siRNA or vs NFAT5 siRNA as indicated, n=4 for all experimental groups). HUASMCs indicates human arterial smooth muscle cells; NFAT5, nuclear factor of activated T‐cells; RPL32, ribosomal protein L3.
Article Snippet: HUASMCs were transfected with short interfering RNA directed against NFAT5 (5′‐ CCA GTT CCT ACA ATG ATA A ‐3′),
Techniques: Migration, Expressing, Recombinant

Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
Article Title: Arterial Wall Stress Controls NFAT5 Activity in Vascular Smooth Muscle Cells
doi: 10.1161/JAHA.113.000626
Figure Lengend Snippet: Validation of tenacin‐C knockdown efficiency. HUASMCs were treated with control siRNA and tenascin‐C (TNC) siRNA. TNC knockdown efficiency (ca. 90%) was verified by Western blot analysis 2 days after siRNA treatment. Note that TNC generates a number of splice variants as evidenced by the 3 to 4 protein bands detected by Western blotting whose intensity was diminished by TNC siRNA treatment. HUASMCs indicates human arterial smooth muscle cells.
Article Snippet: HUASMCs were transfected with short interfering RNA directed against NFAT5 (5′‐ CCA GTT CCT ACA ATG ATA A ‐3′),
Techniques: Western Blot

Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
Article Title: Arterial Wall Stress Controls NFAT5 Activity in Vascular Smooth Muscle Cells
doi: 10.1161/JAHA.113.000626
Figure Lengend Snippet: Hypertension induces NFAT5 translocation and tenascin‐C expression in mouse arteries. Mouse femoral arteries were exposed to normotensive (70 to 50 mm Hg; A, D) and hypertensive (100 to 120 mm Hg; B, E) perfusion conditions. Nuclei were visualized by DAPI staining (A through E, blue fluorescence) and NFAT5 was detected by immunofluorescence analysis (B, red fluorescence, arrows) in cross sections of the arteries. The number of NFAT5‐positive nuclei is increased in high‐pressure perfused arteries (C, *** P <0.001 vs 70 to 50 mm Hg with n=5 for “70 to 50 mm Hg” and n=4 for “120 to 100 mm Hg”). Likewise, the abundance (D through F, red fluorescence, arrow) and mRNA expression (G, real‐time PCR results) of tenascin‐C in the vessel wall is significantly increased under these conditions (F, * P <0.05 vs 70 to 50 mm Hg, n=6 for all experimental groups; scale bar: 100 μm; G, * P <0.05 vs 70 to 50 mm Hg, n=3 for all experimental groups). DAPI indicates 4′,6‐diamidino‐2‐phenylindole; NFAT5, nuclear factor of activated T‐cells; PCR, polymerase chain reaction; TNC, tenascin‐C.
Article Snippet: HUASMCs were transfected with short interfering RNA directed against NFAT5 (5′‐ CCA GTT CCT ACA ATG ATA A ‐3′),
Techniques: Translocation Assay, Expressing, Staining, Fluorescence, Immunofluorescence, Real-time Polymerase Chain Reaction, Polymerase Chain Reaction

Journal: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
Article Title: Arterial Wall Stress Controls NFAT5 Activity in Vascular Smooth Muscle Cells
doi: 10.1161/JAHA.113.000626
Figure Lengend Snippet: Hypertensive perfusion conditions increase the abundance of tenascin‐C in rabbit carotid arteries. Rabbit carotid arteries were exposed to a transmural pressure difference of 20 mm Hg and 150 mm Hg (mimicking hypertension) for 24 hours (Cattaruzza et al. Cell Death Differ . 2002;9:219–226). Tenascin‐C expression was visualized by immunohistochemistry (arrowheads, red staining) in paraffin‐embedded cross sections.
Article Snippet: HUASMCs were transfected with short interfering RNA directed against NFAT5 (5′‐ CCA GTT CCT ACA ATG ATA A ‐3′),
Techniques: Expressing, Immunohistochemistry, Staining