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Proteintech acvr1c
Acvr1c, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 10 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/acvr1c/pm41033083-76-24-26?v=Proteintech
Average 93 stars, based on 10 article reviews
acvr1c - by Bioz Stars, 2026-07
93/100 stars

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( A ) Schematic mKNN graph depicting the analyzed transitions (red lines). ( B ) Violin plots showing example genes critical for aGC function. ( C ) Dot plot exhibiting genes selectively up- and down-regulated in GCmat1. Scales on the right correspond to mean expression levels (color) and to the fraction of nuclei expressing at least one transcript count in the cluster (dot size). ( D ) Violin plots depicting the expression of transcripts that are known to be induced by activity . All data in the figure correspond to dataset 1. ( E ) In situ <t>hybridization</t> reveals the expression of the activity-induced gene Acvr1c in the granule cell layer (GCL). Mice were exposed to an enriched environment for 1 hour (EE) or remained in a home cage (control), and hippocampi were frozen 5 hours later. Representative images depict Acvr1c (pink) expression [4′,6-diamidino-2-phenylindole (DAPI), blue]. Scale bars, 50 μm. Dashed box areas shown on the right panels depict areas of the GCL expressing Acvr1c, which exclude the subgranular zone. ( F ) GCL area occupied by Acvr1c fluorescence in control and EE mice. n = 10 sections per three mice (control) and n = 9 sections per three mice (EE). Asterisk (*) denotes P < 0.05 after Mann-Whitney test. Data depicts means ± SEM.
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( A ) Schematic mKNN graph depicting the analyzed transitions (red lines). ( B ) Violin plots showing example genes critical for aGC function. ( C ) Dot plot exhibiting genes selectively up- and down-regulated in GCmat1. Scales on the right correspond to mean expression levels (color) and to the fraction of nuclei expressing at least one transcript count in the cluster (dot size). ( D ) Violin plots depicting the expression of transcripts that are known to be induced by activity . All data in the figure correspond to dataset 1. ( E ) In situ <t>hybridization</t> reveals the expression of the activity-induced gene Acvr1c in the granule cell layer (GCL). Mice were exposed to an enriched environment for 1 hour (EE) or remained in a home cage (control), and hippocampi were frozen 5 hours later. Representative images depict Acvr1c (pink) expression [4′,6-diamidino-2-phenylindole (DAPI), blue]. Scale bars, 50 μm. Dashed box areas shown on the right panels depict areas of the GCL expressing Acvr1c, which exclude the subgranular zone. ( F ) GCL area occupied by Acvr1c fluorescence in control and EE mice. n = 10 sections per three mice (control) and n = 9 sections per three mice (EE). Asterisk (*) denotes P < 0.05 after Mann-Whitney test. Data depicts means ± SEM.
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ACVR1C is a direct target gene of miR-488-3p. (A) Venn analysis of the target genes of miR-488-3p predicted by TargetScan, miRDB and miRWalk. (B) Venn analysis of the potential target genes of miR-488-3p and upregulated mRNAs in LSCC. (C) Quantitative PCR analysis of the mRNA levels of ACVR1C, ABCA12, TNFSF11 and SYT14 in LSCC cells transfected with miR-488-3p or NC mimics. (D) Western blotting of the protein levels of ACVR1C. (E) Schematic of ACVR1C 3′ UTR sequence containing WT and Mut miR-488-3p binding sites. Luciferase reporter assay measured the luciferase activity of ACVR1C 3′ UTR when FD-LSC-1 cells were transfected with miR-488-3p (F) mimics or (G) inhibitor. ** P<0.01 and *** P<0.001. ACVR1C, activin A receptor type 1C; miR, microRNA; LSCC, laryngeal squamous cell carcinoma; NC, negative control; UTR, untranslated region; WT, wild type; Mut, mutant; N.S., not significant.

Journal: International Journal of Molecular Medicine

Article Title: MEIS1-regulated miR-488-3p suppresses the malignant progression of laryngeal squamous cell carcinoma by targeting ACVR1C

doi: 10.3892/ijmm.2025.5583

Figure Lengend Snippet: ACVR1C is a direct target gene of miR-488-3p. (A) Venn analysis of the target genes of miR-488-3p predicted by TargetScan, miRDB and miRWalk. (B) Venn analysis of the potential target genes of miR-488-3p and upregulated mRNAs in LSCC. (C) Quantitative PCR analysis of the mRNA levels of ACVR1C, ABCA12, TNFSF11 and SYT14 in LSCC cells transfected with miR-488-3p or NC mimics. (D) Western blotting of the protein levels of ACVR1C. (E) Schematic of ACVR1C 3′ UTR sequence containing WT and Mut miR-488-3p binding sites. Luciferase reporter assay measured the luciferase activity of ACVR1C 3′ UTR when FD-LSC-1 cells were transfected with miR-488-3p (F) mimics or (G) inhibitor. ** P<0.01 and *** P<0.001. ACVR1C, activin A receptor type 1C; miR, microRNA; LSCC, laryngeal squamous cell carcinoma; NC, negative control; UTR, untranslated region; WT, wild type; Mut, mutant; N.S., not significant.

Article Snippet: The primary antibodies used were as follows: ACVR1C (1:1,000; cat. no. NBP1-50659; Novus Biologicals, LLC), N-cadherin (1:1,000; cat. no. 13116S; Cell Signaling Technology, Inc.), E-cadherin (1:1,000; cat. no. 3195S; Cell Signaling Technology, Inc.), vimentin (1:1,000; cat. no. 5741S; Cell Signaling Technology, Inc.), Flag (1:1,000; cat. no. F1804; Sigma-Aldrich; Merck KGaA) and GAPDH (1:1,000; cat. no. HC301-02; TransGen Biotech Co., Ltd.).

Techniques: Real-time Polymerase Chain Reaction, Transfection, Western Blot, Sequencing, Binding Assay, Luciferase, Reporter Assay, Activity Assay, Negative Control, Mutagenesis

ACVR1C knockdown inhibits LSCC cell proliferation, migration, invasion and epithelial-mesenchymal transition. (A) Analysis of ACVR1C expression in RNA-seq data ( GSE127165 ). (B) Quantitative PCR and (C) western blot analysis of the mRNA and protein expression levels of ACVR1C in AMC-HN-8 and FD-LSC-1 cells transfected with si-ACVR1C-1 and 2 or si-NC. Cropped images represent different blots, but samples are from the same experiment and the blots were processed in parallel. (D) Cell Counting Kit-8 and (E) colony formation assays investigated the proliferative ability of LSCC cells transfected with si-ACVR1C or si-NC. In the Transwell assay, ACVR1C knockdown significantly suppressed the (F) migration and (G) invasion of LSCC cells. (H) Western blot analysis of the protein levels of E-cadherin, N-cadherin and vimentin in LSCC cells transfected with si-ACVR1C or si-NC. Cropped images represent different blots, but samples are from the same experiment and the blots were processed in parallel. Scale bar, 100 µ m. * P<0.05, ** P<0.01 and *** P<0.001. ACVR1C, activin A receptor type 1C; LSCC, laryngeal squamous cell carcinoma; NC, negative control; si, small interfering RNA.

Journal: International Journal of Molecular Medicine

Article Title: MEIS1-regulated miR-488-3p suppresses the malignant progression of laryngeal squamous cell carcinoma by targeting ACVR1C

doi: 10.3892/ijmm.2025.5583

Figure Lengend Snippet: ACVR1C knockdown inhibits LSCC cell proliferation, migration, invasion and epithelial-mesenchymal transition. (A) Analysis of ACVR1C expression in RNA-seq data ( GSE127165 ). (B) Quantitative PCR and (C) western blot analysis of the mRNA and protein expression levels of ACVR1C in AMC-HN-8 and FD-LSC-1 cells transfected with si-ACVR1C-1 and 2 or si-NC. Cropped images represent different blots, but samples are from the same experiment and the blots were processed in parallel. (D) Cell Counting Kit-8 and (E) colony formation assays investigated the proliferative ability of LSCC cells transfected with si-ACVR1C or si-NC. In the Transwell assay, ACVR1C knockdown significantly suppressed the (F) migration and (G) invasion of LSCC cells. (H) Western blot analysis of the protein levels of E-cadherin, N-cadherin and vimentin in LSCC cells transfected with si-ACVR1C or si-NC. Cropped images represent different blots, but samples are from the same experiment and the blots were processed in parallel. Scale bar, 100 µ m. * P<0.05, ** P<0.01 and *** P<0.001. ACVR1C, activin A receptor type 1C; LSCC, laryngeal squamous cell carcinoma; NC, negative control; si, small interfering RNA.

Article Snippet: The primary antibodies used were as follows: ACVR1C (1:1,000; cat. no. NBP1-50659; Novus Biologicals, LLC), N-cadherin (1:1,000; cat. no. 13116S; Cell Signaling Technology, Inc.), E-cadherin (1:1,000; cat. no. 3195S; Cell Signaling Technology, Inc.), vimentin (1:1,000; cat. no. 5741S; Cell Signaling Technology, Inc.), Flag (1:1,000; cat. no. F1804; Sigma-Aldrich; Merck KGaA) and GAPDH (1:1,000; cat. no. HC301-02; TransGen Biotech Co., Ltd.).

Techniques: Knockdown, Migration, Expressing, RNA Sequencing, Real-time Polymerase Chain Reaction, Western Blot, Transfection, Cell Counting, Transwell Assay, Negative Control, Small Interfering RNA

miR-488-3p suppresses LSCC cell proliferation, migration and invasion by targeting ACVR1C. (A) Western blot analysis of ACVR1C protein in FD-LSC-1 and AMC-HN-8 cells transfected with OE-ACVR1C or control empty plasmid (OE-NC). Flag antibodies were used to detect the Flag-tagged ACVR1C proteins. (B) Western blot analysis of ACVR1C protein expression in FD-LSC-1 and AMC-HN-8 cells co-transfected with OE-NC and NC mimics (Control), OE-NC and miR-488-3p mimics (miR-488-3p mimics), NC mimics and ACVR1C OE (ACVR1C OE) or miR-488-3p mimics and ACVR1C OE (miR-488-3p mimics + ACVR1C OE). (C) Cell Counting Kit-8 and (D) colony formation assays detected the proliferative ability of LSCC cells in different groups. (E and F) Transwell assays determined the migration and invasion of LSCC cells in different groups. Scale bar, 100 µ m. ** P<0.01 and *** P<0.001. ACVR1C, activin A receptor type 1C; miR, microRNA; LSCC, laryngeal squamous cell carcinoma; OE, overexpression.

Journal: International Journal of Molecular Medicine

Article Title: MEIS1-regulated miR-488-3p suppresses the malignant progression of laryngeal squamous cell carcinoma by targeting ACVR1C

doi: 10.3892/ijmm.2025.5583

Figure Lengend Snippet: miR-488-3p suppresses LSCC cell proliferation, migration and invasion by targeting ACVR1C. (A) Western blot analysis of ACVR1C protein in FD-LSC-1 and AMC-HN-8 cells transfected with OE-ACVR1C or control empty plasmid (OE-NC). Flag antibodies were used to detect the Flag-tagged ACVR1C proteins. (B) Western blot analysis of ACVR1C protein expression in FD-LSC-1 and AMC-HN-8 cells co-transfected with OE-NC and NC mimics (Control), OE-NC and miR-488-3p mimics (miR-488-3p mimics), NC mimics and ACVR1C OE (ACVR1C OE) or miR-488-3p mimics and ACVR1C OE (miR-488-3p mimics + ACVR1C OE). (C) Cell Counting Kit-8 and (D) colony formation assays detected the proliferative ability of LSCC cells in different groups. (E and F) Transwell assays determined the migration and invasion of LSCC cells in different groups. Scale bar, 100 µ m. ** P<0.01 and *** P<0.001. ACVR1C, activin A receptor type 1C; miR, microRNA; LSCC, laryngeal squamous cell carcinoma; OE, overexpression.

Article Snippet: The primary antibodies used were as follows: ACVR1C (1:1,000; cat. no. NBP1-50659; Novus Biologicals, LLC), N-cadherin (1:1,000; cat. no. 13116S; Cell Signaling Technology, Inc.), E-cadherin (1:1,000; cat. no. 3195S; Cell Signaling Technology, Inc.), vimentin (1:1,000; cat. no. 5741S; Cell Signaling Technology, Inc.), Flag (1:1,000; cat. no. F1804; Sigma-Aldrich; Merck KGaA) and GAPDH (1:1,000; cat. no. HC301-02; TransGen Biotech Co., Ltd.).

Techniques: Migration, Western Blot, Transfection, Control, Plasmid Preparation, Expressing, Cell Counting, Over Expression

Effect of miR-488-3p on tumor growth in vivo . (A) Image of xenograft tumors after intratumoral injection of miR-488-3p or NC agomir. The xenograft tumor volume was measured to plot the growth curve. (B) Final weight of xenograft tumors. (C) Quantitative PCR analysis of miR-488-3p expression in xenograft tumors. (D) Representative immunohistochemical staining of vimentin, N-cadherin, E-cadherin and Ki-67 expression in xenograft tumors. (E) Schematic representation of the MEIS1/miR-488-3p/ACVR1C axis in regulating laryngeal squamous cell carcinoma progression. The red and green arrows indicate upregulation and downregulation in LSCC, respectively. Scale bar, 50 mm. * P<0.05, ** P<0.01 and *** P<0.001. miR, microRNA; NC, negative control; MEIS1, myeloid ecotropic viral integration site 1; ACVR1C, activin A receptor type 1C.

Journal: International Journal of Molecular Medicine

Article Title: MEIS1-regulated miR-488-3p suppresses the malignant progression of laryngeal squamous cell carcinoma by targeting ACVR1C

doi: 10.3892/ijmm.2025.5583

Figure Lengend Snippet: Effect of miR-488-3p on tumor growth in vivo . (A) Image of xenograft tumors after intratumoral injection of miR-488-3p or NC agomir. The xenograft tumor volume was measured to plot the growth curve. (B) Final weight of xenograft tumors. (C) Quantitative PCR analysis of miR-488-3p expression in xenograft tumors. (D) Representative immunohistochemical staining of vimentin, N-cadherin, E-cadherin and Ki-67 expression in xenograft tumors. (E) Schematic representation of the MEIS1/miR-488-3p/ACVR1C axis in regulating laryngeal squamous cell carcinoma progression. The red and green arrows indicate upregulation and downregulation in LSCC, respectively. Scale bar, 50 mm. * P<0.05, ** P<0.01 and *** P<0.001. miR, microRNA; NC, negative control; MEIS1, myeloid ecotropic viral integration site 1; ACVR1C, activin A receptor type 1C.

Article Snippet: The primary antibodies used were as follows: ACVR1C (1:1,000; cat. no. NBP1-50659; Novus Biologicals, LLC), N-cadherin (1:1,000; cat. no. 13116S; Cell Signaling Technology, Inc.), E-cadherin (1:1,000; cat. no. 3195S; Cell Signaling Technology, Inc.), vimentin (1:1,000; cat. no. 5741S; Cell Signaling Technology, Inc.), Flag (1:1,000; cat. no. F1804; Sigma-Aldrich; Merck KGaA) and GAPDH (1:1,000; cat. no. HC301-02; TransGen Biotech Co., Ltd.).

Techniques: In Vivo, Injection, Real-time Polymerase Chain Reaction, Expressing, Immunohistochemical staining, Staining, Negative Control

( A ) Schematic mKNN graph depicting the analyzed transitions (red lines). ( B ) Violin plots showing example genes critical for aGC function. ( C ) Dot plot exhibiting genes selectively up- and down-regulated in GCmat1. Scales on the right correspond to mean expression levels (color) and to the fraction of nuclei expressing at least one transcript count in the cluster (dot size). ( D ) Violin plots depicting the expression of transcripts that are known to be induced by activity . All data in the figure correspond to dataset 1. ( E ) In situ hybridization reveals the expression of the activity-induced gene Acvr1c in the granule cell layer (GCL). Mice were exposed to an enriched environment for 1 hour (EE) or remained in a home cage (control), and hippocampi were frozen 5 hours later. Representative images depict Acvr1c (pink) expression [4′,6-diamidino-2-phenylindole (DAPI), blue]. Scale bars, 50 μm. Dashed box areas shown on the right panels depict areas of the GCL expressing Acvr1c, which exclude the subgranular zone. ( F ) GCL area occupied by Acvr1c fluorescence in control and EE mice. n = 10 sections per three mice (control) and n = 9 sections per three mice (EE). Asterisk (*) denotes P < 0.05 after Mann-Whitney test. Data depicts means ± SEM.

Journal: Science Advances

Article Title: Transcriptional dynamics orchestrating the development and integration of neurons born in the adult hippocampus

doi: 10.1126/sciadv.adp6039

Figure Lengend Snippet: ( A ) Schematic mKNN graph depicting the analyzed transitions (red lines). ( B ) Violin plots showing example genes critical for aGC function. ( C ) Dot plot exhibiting genes selectively up- and down-regulated in GCmat1. Scales on the right correspond to mean expression levels (color) and to the fraction of nuclei expressing at least one transcript count in the cluster (dot size). ( D ) Violin plots depicting the expression of transcripts that are known to be induced by activity . All data in the figure correspond to dataset 1. ( E ) In situ hybridization reveals the expression of the activity-induced gene Acvr1c in the granule cell layer (GCL). Mice were exposed to an enriched environment for 1 hour (EE) or remained in a home cage (control), and hippocampi were frozen 5 hours later. Representative images depict Acvr1c (pink) expression [4′,6-diamidino-2-phenylindole (DAPI), blue]. Scale bars, 50 μm. Dashed box areas shown on the right panels depict areas of the GCL expressing Acvr1c, which exclude the subgranular zone. ( F ) GCL area occupied by Acvr1c fluorescence in control and EE mice. n = 10 sections per three mice (control) and n = 9 sections per three mice (EE). Asterisk (*) denotes P < 0.05 after Mann-Whitney test. Data depicts means ± SEM.

Article Snippet: Appropriate hybridization probes [Advanced Cell Diagnostics, catalog nos.

Techniques: Expressing, Activity Assay, In Situ Hybridization, Control, Fluorescence, MANN-WHITNEY

( A ) Dot plot exhibiting markers along clusters. Scales on the right correspond to log 2 (mean gene expression) (pseudo-color) and to the fraction of nuclei expressing at least one transcript count in the cluster (dot size). All data corresponds to dataset 1. ( B ) Schematic representation of cells belonging to different clusters (green) distributed within the GCL (purple) and subgranular zone (SGZ; pale blue). Marker genes for each cell state are listed on the right. ( C to H ) In situ hybridization of dentate gyrus sections from 6- or 7-week-old mice. Example of deconvolved images. A distinctive color was assigned to each marker and the specific gene combinations defining cellular states are listed beneath the panels. State 1, 2, or 3 markers are expressed in cells located near the SGZ. State 4 markers are expressed by all mature GCs, not limited to aGCs. Therefore, RNA molecules are distributed throughout the GCL. DAPI (blue) was used to label cell nuclei. Scale bars, 50 μm

Journal: Science Advances

Article Title: Transcriptional dynamics orchestrating the development and integration of neurons born in the adult hippocampus

doi: 10.1126/sciadv.adp6039

Figure Lengend Snippet: ( A ) Dot plot exhibiting markers along clusters. Scales on the right correspond to log 2 (mean gene expression) (pseudo-color) and to the fraction of nuclei expressing at least one transcript count in the cluster (dot size). All data corresponds to dataset 1. ( B ) Schematic representation of cells belonging to different clusters (green) distributed within the GCL (purple) and subgranular zone (SGZ; pale blue). Marker genes for each cell state are listed on the right. ( C to H ) In situ hybridization of dentate gyrus sections from 6- or 7-week-old mice. Example of deconvolved images. A distinctive color was assigned to each marker and the specific gene combinations defining cellular states are listed beneath the panels. State 1, 2, or 3 markers are expressed in cells located near the SGZ. State 4 markers are expressed by all mature GCs, not limited to aGCs. Therefore, RNA molecules are distributed throughout the GCL. DAPI (blue) was used to label cell nuclei. Scale bars, 50 μm

Article Snippet: Appropriate hybridization probes [Advanced Cell Diagnostics, catalog nos.

Techniques: Gene Expression, Expressing, Marker, In Situ Hybridization