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Chem Impex International sodium azide
Sodium Azide, supplied by Chem Impex International, used in various techniques. Bioz Stars score: 95/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/00278/Sodium+azide/pm35298933-124-37-39
Average 95 stars, based on 7 article reviews

sodium azide - by Bioz Stars, 2026-09

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Article Title: End-of-life upcycling of polyurethanes using a room temperature, mechanism-based degradation.
Article Snippet: Isophthaloyl chloride and copper(ii) sulfate pentahydrate were both purchased from Sigma–Aldrich and recrystallized before use (in n-hexane and water, respectively). (2,4,6-Trioxotriazine-1,3,5( 2H,4H,6H)-triyl) tris(hexamethylene) isocyanate (Carbosynth Limited), sodium azide (Chem-Impex International), allyl bromide (Alfa Aesar), 3-chloroperbenzoic acid (75%), pentafluorophenol and 4-(trifluoromethyl)-benzaldehyde (Oakwood Chemical) and 4-nitrobenzaldehyde (AK Scientific) were used as received.

Article Title: Tyrosol Derived Poly(ester-arylate)s for Sustained Drug Delivery from Microparticles.
Article Snippet: New biodegradable polymers are needed for use in drug delivery systems to overcome the high burst release, lack of sustained drug release, and acidic degradation products frequently observed in current formulations.. Commercially available poly(lactide-co-glycolide) (PLGA) is often used for particle drug release formulations; however, it is often limited by its large burst release and acidic degradation products.. Therefore, a biocompatible and biodegradable tyrosol-derived poly(ester-arylate) library has been used to prepare a microparticle drug delivery system which shows sustained delivery of hydrophobic drugs.

Article Title: Electrocatalytic alcohol oxidation by covalently immobilized ruthenium complex on carbon.
Article Snippet: A dearth of discrete immobilized metal complexes exist that electrocatalytically oxidize methanol.. Reported here is the covalent immobilization of a tris(2-pyridylmethyl)amine ruthenium complex [RuII(Cl)(DMSO)(ethynylTPA)] (ethynyl-TPA = (5-ethynyl-2-pyridylmethyl)bis(2-pyridylmethyl)amine) to a glassy carbon (GC) electrode through a CuI catalyzed azide-alkyne cycloaddition (click) reaction between the ethynyl-TPA ligand and an azide derivatized carbon surface forming [RuII(Cl)(DMSO)(GC-click-TPA)]+.. Following water substitution for DMSO and proton coupled electron transfer, [RuIV(O)(Cl)(GC-click-TPA)]+ electrooxidizes alcohols, including methanol, efficiently relative to other immobilized metal complexes.

Article Title: Hydration-mediated effects of saccharide stereochemistry on poly(N -isopropylacrylamide) gel swelling
Article Snippet: To shed new light on the mechanisms of saccharide stereochemistry effect on macromolecules in aqueous solutions, we studied the effect of three monosaccharide stereoisomers, glucose, galactose, and mannose, on the swelling of Poly(N-isopropylacrylamide) (PNIPA) hydrogels.. We equilibrated PNIPA hydrogels in sugar solutions of different concentrations at 25 C, and determined gel volume and mass swelling ratios, and sugar concentration imbalance.. The volume-phase-transition occurred at molal concentrations of 0.587 6 0.004 (galactose), 0.724 6 0.003 (glucose), and 0.846 6 0.004 (mannose).

Article Title: Control of Drug Release from Microparticles by Tuning Their Crystalline Textures: A Structure–Activity Study
Article Snippet: Predicting drug release profiles from polymer microparticles has proven challenging due to the numerous environmental and chemical factors that affect the device and influence the rate of drug release.. By measuring the various polymer properties that can influence drug release, a predictive approach can be used to select polymers with specific properties that will lead to the desired release profile for the application.. To illustrate this, a library of tyrosol-derived poly(ester-arylate)s, poly(amide)s, and poly(carbonate)s were used to evaluate the effects of physical (crystallinity, water accessibility, thermal, and hydrophobicity) and chemical (polymer−drug interactions) polymer properties on the release of a highly crystalline drug dexamethasone, which was loaded at a high weight percent (wt %) in microparticles.

Article Title: Functional phenotyping of hepatic lymphocytes in murine MASH by mass cytometry
Article Snippet: Sodium azide , Chem-Impex Int’l, Inc. , Cat# 00278.

Article Title: Endogenous tyrosinase-catalyzed therapeutics
Article Snippet: Bis(triphenylphosphine) palladium (II) dichloride (Pd (PPh3)2Cl2), sodium azide (NaN3), 4-iodophenol, O-(7-Azabenzotriazol-1-yl)-N, N, Nzzhlxy, Nzzhlxy-tetramethyluronium hexafluorophosphate (HATU), and N-tertbutyloxycarbonyl-6-amino-hexanoic acid were bought from Chem-Impex (Wood Dale, IL, U.S).

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Journal: Nature Communications

Article Title: BRCA1-regulated RRM2 expression protects glioblastoma cells from endogenous replication stress and promotes tumorigenicity

doi: 10.1038/ncomms13398

Figure Lengend Snippet: ( a ) Viability curves for GBM01, GBM02 and GBM03 cells transduced with shCTRL virus or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4) (7 days). ( b ) Quantification of apoptotic cells (% of Annexin V-positive) for GBM01, GBM02 and GBM03 cells transduced with shCTRL virus or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). ( c ) Immunoblot analysis of BRCA1, caspase 3 and cleaved caspase-3 in GBM01 and GBM02 cells transduced with shCTRL virus or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). Tubulin was used as a loading control. ( d ) FACS analysis of cell cycle profile and the proliferative index (% of Edu-positive cells) in GBM01 cells transduced with shCTRL virus or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). ( e ) FACS analysis of cell cycle profile and the mitotic index (% of H3 Ser10 -positive cells) in DMSO or nocodazole treated GBM01 cells transduced with shCTRL virus or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). ( f ) Kaplan-Meier survival curve for NMRI nude mice intracranially injected with GBM01 or GBM03 cells transduced with shCTRL virus or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4 or shBRCA1-5). Statistical significance was calculated by one-way ANOVA, Tukey’s multiple comparisons test ( in vitro study) and Log-rank/Mantel-Cox test ( in vivo study). All data are shown as means±s.d. and performed as technical triplicates. (* P <0.05, ** P <0.005, *** P <0.005, **** P <0.0001; NS represents non-significance).

Article Snippet: The sections were then incubated for 1 h with mouse monoclonal primary antibody against BRCA1 (1:200, IHC-00278, Bethyl Laboratories, Montgomery, TX), RRM2 (1:500, Abcam, ab57653) or Ki67 (DAKO) and followed with Dako EnVision+ Dual Link System-HRP secondary antibody (DAKO, Glostrup, Denmark) incubation for 1 h at room temperature.

Techniques: Transduction, Virus, Western Blot, Control, Injection, In Vitro, In Vivo

( a ) Microscopy analysis and quantification of pRPA mean signal intensity (in S phase) in GBM cells transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). ( b ) Microscopy analysis and quantification of Rad51 mean signal intensity (S phase) in GBM cells transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). ( c ) Microscopy analysis and quantification of 53BP1 foci count (G1 phase) in GBM cells transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). ( d ) Immunoblot analysis of DDR activation in GBM cells transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). * Chk1Ser317; # Chk1Ser345. ( e ) FACS quantification of double-positive p-RPA/γH2AX GBM cells transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). ( f ) FACS quantification of double-positive PCNA/γH2AX GBM cells transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). ( g ) Microscopy analysis and quantification of γH2AXfoci count in GBM cells transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). ( h ) Comet assay and tail moment quantification of DSBs in GBM cells transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). Statistical significance was calculated by one-way ANOVA and Tukey’s multiple comparisons test in a – c , e – h and all data are shown as means ±s.d. and performed as technical triplicates. (* P <0.05, ** P <0.005, *** P <0.005, **** P <0.0001; NS represents non-significance).

Journal: Nature Communications

Article Title: BRCA1-regulated RRM2 expression protects glioblastoma cells from endogenous replication stress and promotes tumorigenicity

doi: 10.1038/ncomms13398

Figure Lengend Snippet: ( a ) Microscopy analysis and quantification of pRPA mean signal intensity (in S phase) in GBM cells transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). ( b ) Microscopy analysis and quantification of Rad51 mean signal intensity (S phase) in GBM cells transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). ( c ) Microscopy analysis and quantification of 53BP1 foci count (G1 phase) in GBM cells transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). ( d ) Immunoblot analysis of DDR activation in GBM cells transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). * Chk1Ser317; # Chk1Ser345. ( e ) FACS quantification of double-positive p-RPA/γH2AX GBM cells transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). ( f ) FACS quantification of double-positive PCNA/γH2AX GBM cells transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). ( g ) Microscopy analysis and quantification of γH2AXfoci count in GBM cells transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). ( h ) Comet assay and tail moment quantification of DSBs in GBM cells transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). Statistical significance was calculated by one-way ANOVA and Tukey’s multiple comparisons test in a – c , e – h and all data are shown as means ±s.d. and performed as technical triplicates. (* P <0.05, ** P <0.005, *** P <0.005, **** P <0.0001; NS represents non-significance).

Techniques: Microscopy, Transduction, Western Blot, Activation Assay, Single Cell Gel Electrophoresis

( a ) DNA fibre assay measuring the replication fork progression speed in GBM cells (GBM01 and GBM02) transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). See also Table 1. ( b ) Replication fork recovery assay showing the quantification of CldU tract length in GBM01 cells transduced with shCTRL or 2 non-overlapping BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4) and treated or not with 2 mM HU (4 h) prior CldU labelling. See also Table 2; . ( c ) Immunoblot analysis of RRM2 protein levels in GBM cells transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). ( d , e ) RT-qPCR analysis of BRCA1 and RRM2 mRNA levels in GBM cells transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). ( f ) FACS analysis of RRM2 protein level changes throughout cell cycle in GBM cells (GBM01) transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). ( g ) Partial sequence of the human RRM2 promoter (GenBank accession number AY032750) , which was used to design Chip primers: P1 primer forward (F)/reverse (R) and P2 primer forward (F)/reverse (R). Positions are numbered from the downstream transcription initiation site (+1). Putative binding sites for transcription factors are color-coded and identified above the sequence. ( h ) Chip immunoprecipitation of BRCA1 binding RRM2 promoter in GBM01-03 cells using primer set P1 and P2. ( i ) Chip immunoprecipitation of BRCA1 binding RRM2 promoter in NHA-DRB and BJ cells using primer set P1 and P2. ( j ) Chip immunoprecipitation of BRCA1 binding RRM2 promoter in PC3, HELA, OVCAR and Cal51 cells using primer set P1 and P2. Statistical significance was calculated by one-way ANOVA and Tukey’s multiple comparisons test in d – f , h – j or Student’s t test ( a , b ) and all data are shown as means±s.d. and performed as technical triplicates. (* P <0.05, ** P <0.005, *** P <0.005, **** P <0.0001; NS represents non-significance).

Journal: Nature Communications

Article Title: BRCA1-regulated RRM2 expression protects glioblastoma cells from endogenous replication stress and promotes tumorigenicity

doi: 10.1038/ncomms13398

Figure Lengend Snippet: ( a ) DNA fibre assay measuring the replication fork progression speed in GBM cells (GBM01 and GBM02) transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). See also Table 1. ( b ) Replication fork recovery assay showing the quantification of CldU tract length in GBM01 cells transduced with shCTRL or 2 non-overlapping BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4) and treated or not with 2 mM HU (4 h) prior CldU labelling. See also Table 2; . ( c ) Immunoblot analysis of RRM2 protein levels in GBM cells transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). ( d , e ) RT-qPCR analysis of BRCA1 and RRM2 mRNA levels in GBM cells transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). ( f ) FACS analysis of RRM2 protein level changes throughout cell cycle in GBM cells (GBM01) transduced with shCTRL or two independent BRCA1-targeting shRNAs (shBRCA1-2 and shBRCA1-4). ( g ) Partial sequence of the human RRM2 promoter (GenBank accession number AY032750) , which was used to design Chip primers: P1 primer forward (F)/reverse (R) and P2 primer forward (F)/reverse (R). Positions are numbered from the downstream transcription initiation site (+1). Putative binding sites for transcription factors are color-coded and identified above the sequence. ( h ) Chip immunoprecipitation of BRCA1 binding RRM2 promoter in GBM01-03 cells using primer set P1 and P2. ( i ) Chip immunoprecipitation of BRCA1 binding RRM2 promoter in NHA-DRB and BJ cells using primer set P1 and P2. ( j ) Chip immunoprecipitation of BRCA1 binding RRM2 promoter in PC3, HELA, OVCAR and Cal51 cells using primer set P1 and P2. Statistical significance was calculated by one-way ANOVA and Tukey’s multiple comparisons test in d – f , h – j or Student’s t test ( a , b ) and all data are shown as means±s.d. and performed as technical triplicates. (* P <0.05, ** P <0.005, *** P <0.005, **** P <0.0001; NS represents non-significance).

Techniques: Transduction, Western Blot, Quantitative RT-PCR, Sequencing, Binding Assay, Immunoprecipitation

( a ) Luciferase assay of transcriptional activation of the RRM2 promoter in GBM01 transduced with shCTRL or shBRCA1-2/shBRCA1-4. ( b ) Luciferase assay of transcriptional activation of the RRM2 promoter in GBM01 after siRNA-mediated knockdown of Sp1; AP-1 and E2F1 in comparison to BRCA1. ( c ) Luciferase assay of transcriptional activation of the RRM2 promoter in GBM01 after siRNA-mediated knockdown of BRCA1 and E2F1 alone or on combination. ( d ) Chip immunoprecipitation of E2F1 binding RRM2 promoter in GBM01 cells using primer set P1 and P2. ( e ) Chip immunoprecipitation of BRCA1 binding RRM2 promoter in GBM01 cells transfected with siCTRL and siE2F1 using primer set P1 and P2. ( f ) DNA fibre assay measuring the replication fork progression speed in GBM cells lacking BRCA1 (shBRCA1-2 and shBRCA1-4) or not (shCTRL) transfected with either control vector (pcDNA) or vector expressing RRM2 (pcDNA-RRM2). See also Table 3. ( g ) Cell viability of GBM cells lacking BRCA1 (shBRCA1-2 and shBRCA1-4) or not (shCTRL) transfected with either control vector (pcDNA) or vector expressing RRM2 (pcDNA-RRM2). ( h ) Immunoblot analysis of BRCA1, p-RPA, RPA and RRM2 in GBM cells lacking BRCA1 (shBRCA1-2 and shBRCA1-4) or not (shCTRL) transfected with either control vector (pcDNA) or vector expressing RRM2 (pcDNA-RRM2). ( i ) Viability-based assessment of EC 50 triapine concentrations in GBM01, GBM02 and GBM03 cells. ( j ) DNA fibre assay measuring the replication fork progression speed in GBM cells treated with DMSO or EC 50 triapine. See also Table 4. Statistical significance was calculated by one-way ANOVA and Tukey’s multiple comparisons test in a – d , f , h or Student’s t test ( e , i ) and all data are shown as means ±s.d. and performed as technical triplicates. (* P <0.05, ** P <0.005, *** P <0.005, **** P <0.0001; NS represents non-significance).

Journal: Nature Communications

Article Title: BRCA1-regulated RRM2 expression protects glioblastoma cells from endogenous replication stress and promotes tumorigenicity

doi: 10.1038/ncomms13398

Figure Lengend Snippet: ( a ) Luciferase assay of transcriptional activation of the RRM2 promoter in GBM01 transduced with shCTRL or shBRCA1-2/shBRCA1-4. ( b ) Luciferase assay of transcriptional activation of the RRM2 promoter in GBM01 after siRNA-mediated knockdown of Sp1; AP-1 and E2F1 in comparison to BRCA1. ( c ) Luciferase assay of transcriptional activation of the RRM2 promoter in GBM01 after siRNA-mediated knockdown of BRCA1 and E2F1 alone or on combination. ( d ) Chip immunoprecipitation of E2F1 binding RRM2 promoter in GBM01 cells using primer set P1 and P2. ( e ) Chip immunoprecipitation of BRCA1 binding RRM2 promoter in GBM01 cells transfected with siCTRL and siE2F1 using primer set P1 and P2. ( f ) DNA fibre assay measuring the replication fork progression speed in GBM cells lacking BRCA1 (shBRCA1-2 and shBRCA1-4) or not (shCTRL) transfected with either control vector (pcDNA) or vector expressing RRM2 (pcDNA-RRM2). See also Table 3. ( g ) Cell viability of GBM cells lacking BRCA1 (shBRCA1-2 and shBRCA1-4) or not (shCTRL) transfected with either control vector (pcDNA) or vector expressing RRM2 (pcDNA-RRM2). ( h ) Immunoblot analysis of BRCA1, p-RPA, RPA and RRM2 in GBM cells lacking BRCA1 (shBRCA1-2 and shBRCA1-4) or not (shCTRL) transfected with either control vector (pcDNA) or vector expressing RRM2 (pcDNA-RRM2). ( i ) Viability-based assessment of EC 50 triapine concentrations in GBM01, GBM02 and GBM03 cells. ( j ) DNA fibre assay measuring the replication fork progression speed in GBM cells treated with DMSO or EC 50 triapine. See also Table 4. Statistical significance was calculated by one-way ANOVA and Tukey’s multiple comparisons test in a – d , f , h or Student’s t test ( e , i ) and all data are shown as means ±s.d. and performed as technical triplicates. (* P <0.05, ** P <0.005, *** P <0.005, **** P <0.0001; NS represents non-significance).

Techniques: Luciferase, Activation Assay, Transduction, Knockdown, Comparison, Immunoprecipitation, Binding Assay, Transfection, Control, Plasmid Preparation, Expressing, Western Blot

( a ) IHC staining of BRCA1 in normal brain (NB), WHO gr. II, III, IV glioma. Shown are representative sections. Scale bar 50 μm. ( b ) Quantification of ( a ) BRCA1 staining. Statistical significance was calculated by one-way ANOVA and Tukey’s multiple comparisons test. ( c ) A survival curve for BRCA1 negative ( n =32); BRCA1 low (< 14.5% of BRCA1 + cells, n =35) or BRCA1 high (>14.5% of BRCA1 + cells, n =78; median survival of 230 days) glioma patients; Log-rank P value=0.00. Median survival for BRCA1 negative and low patient is not available as >50% of patients were alive at the end of study. ( d ) A survival curve for BRCA1 high (>14.5% of BRCA1 + cells, n =60, median survival of 159 days) and BRCA1 low (<14.5% of BRCA1 + cells, n =15; median survival of 251 days) GBM patients. Log-rank P -value=0.293. ( e ) Quantification of RRM2 staining (% of positive cells). Statistical significance was calculated by one-way ANOVA and Tukey’s multiple comparisons test. ( f ) A survival curve for RRM2 negative ( n =64) and RRM2 positive ( n =81; median survival of 222 days) glioma patients, where the median RRM2-positivity is 1% and Log-rank P value=0.00. Median survival for RRM2 negative patients is not available as more than 50% of patients were alive at the end of study. ( g ) A survival curve for RRM2 positive ( n =56, median survival of 148 days) and RRM2 negative ( n =19; median survival of 320 days) GBM patients. Log-rank P value=0.23. ( h ) Spearman correlation test confirmed a positive correlation between the percentage of BRCA1 and RRM2-positive cells in human gliomas (our study dataset). ( i ) Spearman correlation test confirmed a positive correlation between BRCA1 and RRM2 mRNA expression in human gliomas (REMBRANDT dataset). (* P <0.05, ** P <0.005, *** P <0.005, **** P <0.0001; NS represents non-significance).

Journal: Nature Communications

Article Title: BRCA1-regulated RRM2 expression protects glioblastoma cells from endogenous replication stress and promotes tumorigenicity

doi: 10.1038/ncomms13398

Figure Lengend Snippet: ( a ) IHC staining of BRCA1 in normal brain (NB), WHO gr. II, III, IV glioma. Shown are representative sections. Scale bar 50 μm. ( b ) Quantification of ( a ) BRCA1 staining. Statistical significance was calculated by one-way ANOVA and Tukey’s multiple comparisons test. ( c ) A survival curve for BRCA1 negative ( n =32); BRCA1 low (< 14.5% of BRCA1 + cells, n =35) or BRCA1 high (>14.5% of BRCA1 + cells, n =78; median survival of 230 days) glioma patients; Log-rank P value=0.00. Median survival for BRCA1 negative and low patient is not available as >50% of patients were alive at the end of study. ( d ) A survival curve for BRCA1 high (>14.5% of BRCA1 + cells, n =60, median survival of 159 days) and BRCA1 low (<14.5% of BRCA1 + cells, n =15; median survival of 251 days) GBM patients. Log-rank P -value=0.293. ( e ) Quantification of RRM2 staining (% of positive cells). Statistical significance was calculated by one-way ANOVA and Tukey’s multiple comparisons test. ( f ) A survival curve for RRM2 negative ( n =64) and RRM2 positive ( n =81; median survival of 222 days) glioma patients, where the median RRM2-positivity is 1% and Log-rank P value=0.00. Median survival for RRM2 negative patients is not available as more than 50% of patients were alive at the end of study. ( g ) A survival curve for RRM2 positive ( n =56, median survival of 148 days) and RRM2 negative ( n =19; median survival of 320 days) GBM patients. Log-rank P value=0.23. ( h ) Spearman correlation test confirmed a positive correlation between the percentage of BRCA1 and RRM2-positive cells in human gliomas (our study dataset). ( i ) Spearman correlation test confirmed a positive correlation between BRCA1 and RRM2 mRNA expression in human gliomas (REMBRANDT dataset). (* P <0.05, ** P <0.005, *** P <0.005, **** P <0.0001; NS represents non-significance).

Techniques: Immunohistochemistry, Staining, Expressing

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