polyclonal anti alk2 antibody Search Results


gene exp amh mm00431795 g1  (Thermo Fisher)
89
Thermo Fisher gene exp amh mm00431795 g1
Gene Exp Amh Mm00431795 G1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 89/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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rat anti alk2 antibodies  (Sino Biological)
91
Sino Biological rat anti alk2 antibodies
Rat Anti Alk2 Antibodies, supplied by Sino Biological, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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anti alk2  (Boster Bio)
90
Boster Bio anti alk2
Anti Alk2, supplied by Boster Bio, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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anti-alk2 antibody nanobit assay  (Promega)
90
Promega anti-alk2 antibody nanobit assay
Anti Alk2 Antibody Nanobit Assay, supplied by Promega, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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antibodies to smad1 or smad2  (Upstate Biotechnology Inc)
90
Upstate Biotechnology Inc antibodies to smad1 or smad2
Antibodies To Smad1 Or Smad2, supplied by Upstate Biotechnology Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 90 stars, based on 1 article reviews
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mouse anti alk2  (R&D Systems)
90
R&D Systems mouse anti alk2
Mouse Anti Alk2, supplied by R&D Systems, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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phosphorylated human ampkα2 β2 γ1  (Carna Inc)
96
Carna Inc phosphorylated human ampkα2 β2 γ1
Phosphorylated Human Ampkα2 β2 γ1, supplied by Carna Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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anti alk2  (Santa Cruz Biotechnology)
91
Santa Cruz Biotechnology anti alk2
Anti Alk2, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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anti goat for acvr1 antibodies  (Jackson Immuno)
98
Jackson Immuno anti goat for acvr1 antibodies
Figure 2. <t>ACVR1</t> (a,a’), BMPR1A (b,b’), BMPR1B (c,c’), and TGFBR1 (d,d’) mRNA and protein abundance in preantral (primordial, primary, and secondary follicles) and small antral follicles obtained from the control (CTR) and methoxychlor (MXC-) treated gilts. The mRNA expression (quantitative real-time PCR) is presented relative to GAPDH as mean ± SEM (a–d). Relative protein abundance was measured by the densitometric method and expressed as the ratio relative to β-actin abundance (mean ± SEM, a’–d’). The fragment of membranes with bands corresponding to predicted molecular weights is shown above graphs. Asterisks denote significant differences between the CTR and treated animals (for preantral follicles pool n = 5, for small antral follicle n = 15, * p < 0.05, ** p < 0.01, *** p < 0.001, Mann–Whitney U test).
Anti Goat For Acvr1 Antibodies, supplied by Jackson Immuno, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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anti alk2  (R&D Systems)
92
R&D Systems anti alk2
Figure 2. <t>ACVR1</t> (a,a’), BMPR1A (b,b’), BMPR1B (c,c’), and TGFBR1 (d,d’) mRNA and protein abundance in preantral (primordial, primary, and secondary follicles) and small antral follicles obtained from the control (CTR) and methoxychlor (MXC-) treated gilts. The mRNA expression (quantitative real-time PCR) is presented relative to GAPDH as mean ± SEM (a–d). Relative protein abundance was measured by the densitometric method and expressed as the ratio relative to β-actin abundance (mean ± SEM, a’–d’). The fragment of membranes with bands corresponding to predicted molecular weights is shown above graphs. Asterisks denote significant differences between the CTR and treated animals (for preantral follicles pool n = 5, for small antral follicle n = 15, * p < 0.05, ** p < 0.01, *** p < 0.001, Mann–Whitney U test).
Anti Alk2, supplied by R&D Systems, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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rabbit anti acvr1  (Cell Signaling Technology Inc)
97
Cell Signaling Technology Inc rabbit anti acvr1
Figure 2. <t>ACVR1</t> (a,a’), BMPR1A (b,b’), BMPR1B (c,c’), and TGFBR1 (d,d’) mRNA and protein abundance in preantral (primordial, primary, and secondary follicles) and small antral follicles obtained from the control (CTR) and methoxychlor (MXC-) treated gilts. The mRNA expression (quantitative real-time PCR) is presented relative to GAPDH as mean ± SEM (a–d). Relative protein abundance was measured by the densitometric method and expressed as the ratio relative to β-actin abundance (mean ± SEM, a’–d’). The fragment of membranes with bands corresponding to predicted molecular weights is shown above graphs. Asterisks denote significant differences between the CTR and treated animals (for preantral follicles pool n = 5, for small antral follicle n = 15, * p < 0.05, ** p < 0.01, *** p < 0.001, Mann–Whitney U test).
Rabbit Anti Acvr1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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anti mouse acvr1  (Proteintech)
93
Proteintech anti mouse acvr1
( A ) Schematic diagram depicting the generation of <t>Acvr1</t> R206H/+ flox mice using CRISPR-Cas9 technology. ( B ) microCT showing spontaneous HO formation around the joints of Prrx1-Cre ; Acvr1 R206H/+ mice, but not Prrx1-Cre mice. ( C , D ) Representative microCT image ( C ) and statistical analysis ( D ) of HO formation in the tibial muscle of Tek -Cre ; Acvr1 R206H/+ mice, but not Tek -Cre mice after CTX injury ( n = 4 per group). **** P = 6.05e-7. ( E , F ) Representative HE staining ( E) and safranine O staining ( F ) images of the injured tendon of Gli1-CreER T2 and Gli1-CreER T2 ; Acvr1 R206H/+ mice at 7 dpi. Scale bar, 200 μm. ( G ) Statistical analysis of Safranine O + region in injured tendon of Gli1-CreER T2 and Gli1-CreER T2 ; Acvr1 R206H/+ mice at 7 dpi ( n = 5 per group). **** P = 2.28e-6. ( H ) Statistical analysis of HO volume in the injured tendon of Gli1-CreER T2 and Gli1-CreER T2 ; Acvr1 R206H/+ mice at 56 dpi ( n = 5 per group). **** P = 1.29e-5. ( I ) Representative microCT images of HO in the injured tendon of Gli1-CreER T2 and Gli1-CreER T2 ; Acvr1 R206H/+ mice at 56 dpi. ( J , K ) Statistical analysis ( J ) and representative immunofluorescence images ( K ) of Gli1 + cells in the injured tendon of Gli1-CreER T2 ; Ai9 and Gli1-CreER T2 ; Ai9; Acvr1 R206H/+ mice at 3, 5, and 7 dpi ( n = 5 per group). * P = 3.86e-2, ** P = 3.82e-3, **** P = 2.73e-4. Scale bar, 100 μm. Data are represented as the mean ± SD. All P values were determined by unpaired Student’s t test.
Anti Mouse Acvr1, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


Figure 2. ACVR1 (a,a’), BMPR1A (b,b’), BMPR1B (c,c’), and TGFBR1 (d,d’) mRNA and protein abundance in preantral (primordial, primary, and secondary follicles) and small antral follicles obtained from the control (CTR) and methoxychlor (MXC-) treated gilts. The mRNA expression (quantitative real-time PCR) is presented relative to GAPDH as mean ± SEM (a–d). Relative protein abundance was measured by the densitometric method and expressed as the ratio relative to β-actin abundance (mean ± SEM, a’–d’). The fragment of membranes with bands corresponding to predicted molecular weights is shown above graphs. Asterisks denote significant differences between the CTR and treated animals (for preantral follicles pool n = 5, for small antral follicle n = 15, * p < 0.05, ** p < 0.01, *** p < 0.001, Mann–Whitney U test).

Journal: International journal of molecular sciences

Article Title: Long-Term Changes in Ovarian Follicles of Gilts Exposed Neonatally to Methoxychlor: Effects on Oocyte-Derived Factors, Anti-Müllerian Hormone, Follicle-Stimulating Hormone, and Cognate Receptors.

doi: 10.3390/ijms23052780

Figure Lengend Snippet: Figure 2. ACVR1 (a,a’), BMPR1A (b,b’), BMPR1B (c,c’), and TGFBR1 (d,d’) mRNA and protein abundance in preantral (primordial, primary, and secondary follicles) and small antral follicles obtained from the control (CTR) and methoxychlor (MXC-) treated gilts. The mRNA expression (quantitative real-time PCR) is presented relative to GAPDH as mean ± SEM (a–d). Relative protein abundance was measured by the densitometric method and expressed as the ratio relative to β-actin abundance (mean ± SEM, a’–d’). The fragment of membranes with bands corresponding to predicted molecular weights is shown above graphs. Asterisks denote significant differences between the CTR and treated animals (for preantral follicles pool n = 5, for small antral follicle n = 15, * p < 0.05, ** p < 0.01, *** p < 0.001, Mann–Whitney U test).

Article Snippet: Next, the membranes were incubated for 1 h at room temperature with secondary anti-rabbit (in the case of AMH, AMHR2, BMP15, BMPR1A, BMPR1B, BMPR2, FSHR, GDF9, and TGFBR1) or anti-goat (for ACVR1) antibodies linked to horseradish peroxidase (Jackson ImmunoResearch, Cambridge, UK) at 1:10000 antibody dilution.

Techniques: Quantitative Proteomics, Control, Expressing, Real-time Polymerase Chain Reaction, MANN-WHITNEY

Figure 3. Immunolocalization of ACVR1, BMPR1A, BMPR1B, and TGFBR1 in preantral (primordial, primary, and secondary follicle) (a) and small antral (b) follicles of the control (CTR) and methoxychlor (MXC-) treated gilts. ACVR1, BMPR1A, BMPR1B, and TGFBR1 positive staining was observed in oocytes (asterisks) and granulosa cells (arrows) of preantral follicles, as well as granulosa (arrows) and theca cells (arrowheads) of small antral follicles, in both examined groups. All sections were counterstained with hematoxylin QS. There was no positive staining observed in the negative control sections (a,b, insets). Prim—primordial follicles; SF—secondary follicles; AF—antral follicles. Bars = 50 µm.

Journal: International journal of molecular sciences

Article Title: Long-Term Changes in Ovarian Follicles of Gilts Exposed Neonatally to Methoxychlor: Effects on Oocyte-Derived Factors, Anti-Müllerian Hormone, Follicle-Stimulating Hormone, and Cognate Receptors.

doi: 10.3390/ijms23052780

Figure Lengend Snippet: Figure 3. Immunolocalization of ACVR1, BMPR1A, BMPR1B, and TGFBR1 in preantral (primordial, primary, and secondary follicle) (a) and small antral (b) follicles of the control (CTR) and methoxychlor (MXC-) treated gilts. ACVR1, BMPR1A, BMPR1B, and TGFBR1 positive staining was observed in oocytes (asterisks) and granulosa cells (arrows) of preantral follicles, as well as granulosa (arrows) and theca cells (arrowheads) of small antral follicles, in both examined groups. All sections were counterstained with hematoxylin QS. There was no positive staining observed in the negative control sections (a,b, insets). Prim—primordial follicles; SF—secondary follicles; AF—antral follicles. Bars = 50 µm.

Article Snippet: Next, the membranes were incubated for 1 h at room temperature with secondary anti-rabbit (in the case of AMH, AMHR2, BMP15, BMPR1A, BMPR1B, BMPR2, FSHR, GDF9, and TGFBR1) or anti-goat (for ACVR1) antibodies linked to horseradish peroxidase (Jackson ImmunoResearch, Cambridge, UK) at 1:10000 antibody dilution.

Techniques: Control, Staining, Negative Control

( A ) Schematic diagram depicting the generation of Acvr1 R206H/+ flox mice using CRISPR-Cas9 technology. ( B ) microCT showing spontaneous HO formation around the joints of Prrx1-Cre ; Acvr1 R206H/+ mice, but not Prrx1-Cre mice. ( C , D ) Representative microCT image ( C ) and statistical analysis ( D ) of HO formation in the tibial muscle of Tek -Cre ; Acvr1 R206H/+ mice, but not Tek -Cre mice after CTX injury ( n = 4 per group). **** P = 6.05e-7. ( E , F ) Representative HE staining ( E) and safranine O staining ( F ) images of the injured tendon of Gli1-CreER T2 and Gli1-CreER T2 ; Acvr1 R206H/+ mice at 7 dpi. Scale bar, 200 μm. ( G ) Statistical analysis of Safranine O + region in injured tendon of Gli1-CreER T2 and Gli1-CreER T2 ; Acvr1 R206H/+ mice at 7 dpi ( n = 5 per group). **** P = 2.28e-6. ( H ) Statistical analysis of HO volume in the injured tendon of Gli1-CreER T2 and Gli1-CreER T2 ; Acvr1 R206H/+ mice at 56 dpi ( n = 5 per group). **** P = 1.29e-5. ( I ) Representative microCT images of HO in the injured tendon of Gli1-CreER T2 and Gli1-CreER T2 ; Acvr1 R206H/+ mice at 56 dpi. ( J , K ) Statistical analysis ( J ) and representative immunofluorescence images ( K ) of Gli1 + cells in the injured tendon of Gli1-CreER T2 ; Ai9 and Gli1-CreER T2 ; Ai9; Acvr1 R206H/+ mice at 3, 5, and 7 dpi ( n = 5 per group). * P = 3.86e-2, ** P = 3.82e-3, **** P = 2.73e-4. Scale bar, 100 μm. Data are represented as the mean ± SD. All P values were determined by unpaired Student’s t test.

Journal: The EMBO Journal

Article Title: GNAS/PKA signaling promotes aberrant osteochondral differentiation of Gli1 + tendon sheath progenitors

doi: 10.1038/s44318-025-00553-7

Figure Lengend Snippet: ( A ) Schematic diagram depicting the generation of Acvr1 R206H/+ flox mice using CRISPR-Cas9 technology. ( B ) microCT showing spontaneous HO formation around the joints of Prrx1-Cre ; Acvr1 R206H/+ mice, but not Prrx1-Cre mice. ( C , D ) Representative microCT image ( C ) and statistical analysis ( D ) of HO formation in the tibial muscle of Tek -Cre ; Acvr1 R206H/+ mice, but not Tek -Cre mice after CTX injury ( n = 4 per group). **** P = 6.05e-7. ( E , F ) Representative HE staining ( E) and safranine O staining ( F ) images of the injured tendon of Gli1-CreER T2 and Gli1-CreER T2 ; Acvr1 R206H/+ mice at 7 dpi. Scale bar, 200 μm. ( G ) Statistical analysis of Safranine O + region in injured tendon of Gli1-CreER T2 and Gli1-CreER T2 ; Acvr1 R206H/+ mice at 7 dpi ( n = 5 per group). **** P = 2.28e-6. ( H ) Statistical analysis of HO volume in the injured tendon of Gli1-CreER T2 and Gli1-CreER T2 ; Acvr1 R206H/+ mice at 56 dpi ( n = 5 per group). **** P = 1.29e-5. ( I ) Representative microCT images of HO in the injured tendon of Gli1-CreER T2 and Gli1-CreER T2 ; Acvr1 R206H/+ mice at 56 dpi. ( J , K ) Statistical analysis ( J ) and representative immunofluorescence images ( K ) of Gli1 + cells in the injured tendon of Gli1-CreER T2 ; Ai9 and Gli1-CreER T2 ; Ai9; Acvr1 R206H/+ mice at 3, 5, and 7 dpi ( n = 5 per group). * P = 3.86e-2, ** P = 3.82e-3, **** P = 2.73e-4. Scale bar, 100 μm. Data are represented as the mean ± SD. All P values were determined by unpaired Student’s t test.

Article Snippet: Anti-mouse ACVR1 , Proteintech , Cat#67417-1-Ig.

Techniques: CRISPR, Staining, Immunofluorescence

( A , B ) Representative immunofluorescence and statistical analysis of GLI1 and ACVR1 in injured site of Gli1-CreER T2 ; Ai9 and Gli1-CreER T2 ; Ai9; Acvr1 R206H/+ mice at 5 dpi ( n = 5 per group). P = 5.18e-1. N.S. indicated no significance. Scale bar, 100:μm. ( C , D ) Representative immunofluorescence and statistical analysis of GLI1 and p-SMAD1/5 in injured site of Gli1-CreER T2 ; Ai9 and Gli1-CreER T2 ; Ai9; Acvr1 R206H/+ mice at 5 dpi ( n = 5 per group). **** P = 6.89e-6. Scale bar, 100 μm. ( E ) Sanger sequencing showed that the STOP cassette preceding the Acvr1 R206H/+ mutation was disrupted. Data is presented as mean ± SD. All P values were determined by unpaired Student’s t test.

Journal: The EMBO Journal

Article Title: GNAS/PKA signaling promotes aberrant osteochondral differentiation of Gli1 + tendon sheath progenitors

doi: 10.1038/s44318-025-00553-7

Figure Lengend Snippet: ( A , B ) Representative immunofluorescence and statistical analysis of GLI1 and ACVR1 in injured site of Gli1-CreER T2 ; Ai9 and Gli1-CreER T2 ; Ai9; Acvr1 R206H/+ mice at 5 dpi ( n = 5 per group). P = 5.18e-1. N.S. indicated no significance. Scale bar, 100:μm. ( C , D ) Representative immunofluorescence and statistical analysis of GLI1 and p-SMAD1/5 in injured site of Gli1-CreER T2 ; Ai9 and Gli1-CreER T2 ; Ai9; Acvr1 R206H/+ mice at 5 dpi ( n = 5 per group). **** P = 6.89e-6. Scale bar, 100 μm. ( E ) Sanger sequencing showed that the STOP cassette preceding the Acvr1 R206H/+ mutation was disrupted. Data is presented as mean ± SD. All P values were determined by unpaired Student’s t test.

Article Snippet: Anti-mouse ACVR1 , Proteintech , Cat#67417-1-Ig.

Techniques: Immunofluorescence, Sequencing, Mutagenesis

( A , B ) Representative immunofluorescence images ( A ) and statistical analysis of frequency ( B ) of GLI1 - / FMOD - , GLI1 + / FMOD - , GLI1 + / FMOD + , GLI1 - / FMOD + cells in the injured site of FOP model mice at 3 dpi ( n = 5 per group). P values from left to right: ** P = 2.27e-3, **** P = 1.17e-12, *** P = 4.59e-4, **** P = 6.94e-13, **** P = 2.49e-11. Scale bar, 200 or 20 μm. ( C, D ) Representative immunofluorescence images ( C ) and statistical analysis of frequency ( D ) of GLI1 - / SOX9 - , GLI1 + /SOX9 − , GLI1 − /SOX9 + , GLI1 + / SOX9 + cells in the injured site of FOP model mice at 5 dpi ( n = 5 per group). P values from left to right: * P = 2.52e-2, * P = 1.85e-2, **** P = 3.43e-5, *** P = 4.18e-4. Scale bar, 200 or 20 μm. ( E , F ) Representative immunofluorescence images ( E ) and statistical analysis of frequency ( F ) of GLI1 − /RUNX2 - , GLI1 + /RUNX2 − , GLI1 − /RUNX2 + , GLI1 + /RUNX2 + cells in the injured site of FOP model mice at 5 dpi ( n = 5 per group). P values from left to right: **** P = 5.56e-5, **** P = 1.32e-6, ** P = 1.12e-3, **** P = 1.73e-5. Scale bar, 200 or 20 μm. ( G , H ) Representative immunofluorescence images ( G ) and statistical analysis of frequency ( H ) of GLI1 - /COL2 - , GLI1 + / COL2 − , GLI1 + / COL2 + , GLI1 - / COL2 + cells in the injured site of FOP model mice at 7 dpi ( n = 5 per group). P values from left to right: **** P = 1.52e-10, **** P = 2.90e-11, **** P = 6.99e-11. Scale bar, 200 or 20 μm. ( I ) Representative immunofluorescence images showing Gli1 + tendon sheath progenitors differentiate into osteocytes at 14 dpi in FOP model mice. Scale bar, 200 or 20 μm. ( J ) Statistical analysis of the frequency of GLI1 - /OCN - , GLI1 + /OCN + , GLI1 - /OCN + , GLI1 + /OCN - cells in the injured site of FOP model mice at 14 dpi ( n = 5 per group). P values from left to right: **** P = 8.87e-11, **** P = 9.49e-7, **** P = 4.35e-10, **** P = 3.85e-6, **** P = 6.35e-5. ( K , L ) Representative Safranine O staining images ( K ) and statistical analysis ( L ) of chondrocyte region in the injured tendon of Gli1 - CreER T2 ; Acvr1 R206H/+ and Gli1 - CreER T2 ; Acvr1 R206H/+ ; DTA mice ( n = 5 per group). *** P = 3.27e-4. Scale bar, 200 μm. ( M , N ) Representative microCT images ( M ) and statistical analysis ( N ) of HO in the injured tendon of Gli1 - Cre ERT2 ; Acvr1 R206H/+ and Gli1 - Cre ERT2 ; Acvr1 R206H/+ ; DTA mice at 63 dpi ( n = 5 per group). **** P = 7.86e-7. Data are presented as mean ± SD. All P values were determined by One-way ANOVA with Bonferroni post hoc test ( B , D , F , H , J ) and unpaired Student’s t test ( L , N ).

Journal: The EMBO Journal

Article Title: GNAS/PKA signaling promotes aberrant osteochondral differentiation of Gli1 + tendon sheath progenitors

doi: 10.1038/s44318-025-00553-7

Figure Lengend Snippet: ( A , B ) Representative immunofluorescence images ( A ) and statistical analysis of frequency ( B ) of GLI1 - / FMOD - , GLI1 + / FMOD - , GLI1 + / FMOD + , GLI1 - / FMOD + cells in the injured site of FOP model mice at 3 dpi ( n = 5 per group). P values from left to right: ** P = 2.27e-3, **** P = 1.17e-12, *** P = 4.59e-4, **** P = 6.94e-13, **** P = 2.49e-11. Scale bar, 200 or 20 μm. ( C, D ) Representative immunofluorescence images ( C ) and statistical analysis of frequency ( D ) of GLI1 - / SOX9 - , GLI1 + /SOX9 − , GLI1 − /SOX9 + , GLI1 + / SOX9 + cells in the injured site of FOP model mice at 5 dpi ( n = 5 per group). P values from left to right: * P = 2.52e-2, * P = 1.85e-2, **** P = 3.43e-5, *** P = 4.18e-4. Scale bar, 200 or 20 μm. ( E , F ) Representative immunofluorescence images ( E ) and statistical analysis of frequency ( F ) of GLI1 − /RUNX2 - , GLI1 + /RUNX2 − , GLI1 − /RUNX2 + , GLI1 + /RUNX2 + cells in the injured site of FOP model mice at 5 dpi ( n = 5 per group). P values from left to right: **** P = 5.56e-5, **** P = 1.32e-6, ** P = 1.12e-3, **** P = 1.73e-5. Scale bar, 200 or 20 μm. ( G , H ) Representative immunofluorescence images ( G ) and statistical analysis of frequency ( H ) of GLI1 - /COL2 - , GLI1 + / COL2 − , GLI1 + / COL2 + , GLI1 - / COL2 + cells in the injured site of FOP model mice at 7 dpi ( n = 5 per group). P values from left to right: **** P = 1.52e-10, **** P = 2.90e-11, **** P = 6.99e-11. Scale bar, 200 or 20 μm. ( I ) Representative immunofluorescence images showing Gli1 + tendon sheath progenitors differentiate into osteocytes at 14 dpi in FOP model mice. Scale bar, 200 or 20 μm. ( J ) Statistical analysis of the frequency of GLI1 - /OCN - , GLI1 + /OCN + , GLI1 - /OCN + , GLI1 + /OCN - cells in the injured site of FOP model mice at 14 dpi ( n = 5 per group). P values from left to right: **** P = 8.87e-11, **** P = 9.49e-7, **** P = 4.35e-10, **** P = 3.85e-6, **** P = 6.35e-5. ( K , L ) Representative Safranine O staining images ( K ) and statistical analysis ( L ) of chondrocyte region in the injured tendon of Gli1 - CreER T2 ; Acvr1 R206H/+ and Gli1 - CreER T2 ; Acvr1 R206H/+ ; DTA mice ( n = 5 per group). *** P = 3.27e-4. Scale bar, 200 μm. ( M , N ) Representative microCT images ( M ) and statistical analysis ( N ) of HO in the injured tendon of Gli1 - Cre ERT2 ; Acvr1 R206H/+ and Gli1 - Cre ERT2 ; Acvr1 R206H/+ ; DTA mice at 63 dpi ( n = 5 per group). **** P = 7.86e-7. Data are presented as mean ± SD. All P values were determined by One-way ANOVA with Bonferroni post hoc test ( B , D , F , H , J ) and unpaired Student’s t test ( L , N ).

Article Snippet: Anti-mouse ACVR1 , Proteintech , Cat#67417-1-Ig.

Techniques: Immunofluorescence, Staining

( A – D ) Representative immunofluorescence images of GNAS expression in uninjured tendons ( A ) and injured sites of Gli1 - CreER T2 ; Ai9 mice at 5 ( B ), 7 ( C ) and 14 ( D ) dpi. Scale bar, 50 μm. ( E , F ) Statistical analysis of GNAS + region ( E ) and GNAS + /GLI1 + region ( F ) in uninjured tendons and injured sites of Gli1 - CreER T2 ; Acvr1 R206H/+ mice at 5, 7 and 14 dpi ( n = 5 per group). P values from left to right: **** P = 8.29e-10, **** P = 1.16e-8, **** P = 1.57e-8. **** P = 2.36e-9, **** P = 1.71e-6, **** P = 9.06e-6. ( G , H ) Statistical analysis of p-PKA substrate + region ( G ) and p-PKA substrate + /GLI1 + region ( H ) in uninjured tendons and injured sites of Gli1 - CreER T2 ; Acvr1 R206H/+ mice at 5, 7 and 14 dpi ( n = 5 per group). P values from left to right: **** P = 1.42e-6, **** P = 7.23e-6, **** P = 1.53e-5. **** P = 1.96e-5, ** P = 2.63e-3, **** P = 6.44e-4. ( I – L ) Representative immunofluorescence images of p-PKA substrate expression in uninjured tendons ( I ) and injured sites of Gli1 - CreER T2 ; Acvr1 R206H/+ mice at 5 ( J ), 7 ( K ) and 14 ( L ) dpi. Scale bar, 50 μm. Data is presented as mean ± SD. All P values were determined by unpaired Student’s t test.

Journal: The EMBO Journal

Article Title: GNAS/PKA signaling promotes aberrant osteochondral differentiation of Gli1 + tendon sheath progenitors

doi: 10.1038/s44318-025-00553-7

Figure Lengend Snippet: ( A – D ) Representative immunofluorescence images of GNAS expression in uninjured tendons ( A ) and injured sites of Gli1 - CreER T2 ; Ai9 mice at 5 ( B ), 7 ( C ) and 14 ( D ) dpi. Scale bar, 50 μm. ( E , F ) Statistical analysis of GNAS + region ( E ) and GNAS + /GLI1 + region ( F ) in uninjured tendons and injured sites of Gli1 - CreER T2 ; Acvr1 R206H/+ mice at 5, 7 and 14 dpi ( n = 5 per group). P values from left to right: **** P = 8.29e-10, **** P = 1.16e-8, **** P = 1.57e-8. **** P = 2.36e-9, **** P = 1.71e-6, **** P = 9.06e-6. ( G , H ) Statistical analysis of p-PKA substrate + region ( G ) and p-PKA substrate + /GLI1 + region ( H ) in uninjured tendons and injured sites of Gli1 - CreER T2 ; Acvr1 R206H/+ mice at 5, 7 and 14 dpi ( n = 5 per group). P values from left to right: **** P = 1.42e-6, **** P = 7.23e-6, **** P = 1.53e-5. **** P = 1.96e-5, ** P = 2.63e-3, **** P = 6.44e-4. ( I – L ) Representative immunofluorescence images of p-PKA substrate expression in uninjured tendons ( I ) and injured sites of Gli1 - CreER T2 ; Acvr1 R206H/+ mice at 5 ( J ), 7 ( K ) and 14 ( L ) dpi. Scale bar, 50 μm. Data is presented as mean ± SD. All P values were determined by unpaired Student’s t test.

Article Snippet: Anti-mouse ACVR1 , Proteintech , Cat#67417-1-Ig.

Techniques: Immunofluorescence, Expressing

( A , B ) Representative immunofluorescence images ( A ) and statistical analysis ( B ) of SOX9 + region in injured site from tenotomized mice following vehicle and NF449 treatment ( n = 5 per group). *** P = 8.94e-4. Scale bar, 10 μm. ( C , D ) Representative immunofluorescence images ( C ) and statistical analysis ( D ) of RUNX2 + region in injured site from tenotomized mice following vehicle and NF449 treatment ( n = 5 per group). * P = 1.37e-2. Scale bar, 10 μm. ( E , F ) Representative Safranine O staining images ( E ) and statistical analysis ( F ) of Safranine O + region in injured site from tenotomized mice following vehicle and NF449 treatment ( n = 5 per group). ** P = 1.85e-3. Scale bar, 100 μm. ( G , H ) Representative microCT images ( G ) and statistical analysis ( H ) of HO volume in injured site from tenotomized mice following vehicle and NF449 treatment ( n = 5 per group). *** P = 1.39e-4. ( I , J ) Representative Safranine O staining images ( I ) and statistical analysis ( J ) of Safranine O + region in injured site from tenotomized Gli1-CreER T2 and Gli1-CreER T2 ; Prkaca f/f mice ( n = 5 per group). *** P = 1.18e-4. Scale bar, 100 μm. ( K , L ) Representative microCT images ( K ) and statistical analysis ( L ) of HO volume in injured site from tenotomized Gli1-CreER T2 and Gli1-CreER T2 ; Prkaca f/f mice ( n = 5 per group). *** P = 5.11e-4. ( M , N ) Representative Safranine O staining images ( M ) and statistical analysis ( N ) of Safranine O + region in injured site from tenotomized Gli1-CreER T2 ; Acvr1 R206H/+ mice following vehicle and NF449 treatment ( n = 5 per group). **** P = 1.5e-7. Scale bar, 100 μm. ( O , P ) Representative microCT images ( O ) and statistical analysis ( P ) of HO volume in injured site from tenotomized Gli1-CreER T2 ; Acvr1 R206H/+ mice following vehicle and NF449 treatment ( n = 5 per group). **** P = 3.87e-6. ( Q , R ) Representative Safranine O staining images ( Q ) and statistical analysis ( R ) of Safranine O + region in injured site from tenotomized Gli1-CreER T2 ; Acvr1 R206H/+ and Gli1-CreER T2 ; Acvr1 R206H/+ ; Prkaca f/f mice at 7 dpi ( n = 5 per group). **** P = 6.2e-7. Scale bar, 100 μm. ( S , T ) Representative microCT images ( S ) and statistical analysis ( T ) of HO volume in injured site from tenotomized Gli1-CreER T2 ; Acvr1 R206H/+ and Gli1-CreER T2 ; Acvr1 R206H/+ ; Prkaca f/f mice at 14 dpi ( n = 5 per group). *** P = 1.79e-4. Data are presented as mean ± SD. All P values were determined by unpaired Student’s t test.

Journal: The EMBO Journal

Article Title: GNAS/PKA signaling promotes aberrant osteochondral differentiation of Gli1 + tendon sheath progenitors

doi: 10.1038/s44318-025-00553-7

Figure Lengend Snippet: ( A , B ) Representative immunofluorescence images ( A ) and statistical analysis ( B ) of SOX9 + region in injured site from tenotomized mice following vehicle and NF449 treatment ( n = 5 per group). *** P = 8.94e-4. Scale bar, 10 μm. ( C , D ) Representative immunofluorescence images ( C ) and statistical analysis ( D ) of RUNX2 + region in injured site from tenotomized mice following vehicle and NF449 treatment ( n = 5 per group). * P = 1.37e-2. Scale bar, 10 μm. ( E , F ) Representative Safranine O staining images ( E ) and statistical analysis ( F ) of Safranine O + region in injured site from tenotomized mice following vehicle and NF449 treatment ( n = 5 per group). ** P = 1.85e-3. Scale bar, 100 μm. ( G , H ) Representative microCT images ( G ) and statistical analysis ( H ) of HO volume in injured site from tenotomized mice following vehicle and NF449 treatment ( n = 5 per group). *** P = 1.39e-4. ( I , J ) Representative Safranine O staining images ( I ) and statistical analysis ( J ) of Safranine O + region in injured site from tenotomized Gli1-CreER T2 and Gli1-CreER T2 ; Prkaca f/f mice ( n = 5 per group). *** P = 1.18e-4. Scale bar, 100 μm. ( K , L ) Representative microCT images ( K ) and statistical analysis ( L ) of HO volume in injured site from tenotomized Gli1-CreER T2 and Gli1-CreER T2 ; Prkaca f/f mice ( n = 5 per group). *** P = 5.11e-4. ( M , N ) Representative Safranine O staining images ( M ) and statistical analysis ( N ) of Safranine O + region in injured site from tenotomized Gli1-CreER T2 ; Acvr1 R206H/+ mice following vehicle and NF449 treatment ( n = 5 per group). **** P = 1.5e-7. Scale bar, 100 μm. ( O , P ) Representative microCT images ( O ) and statistical analysis ( P ) of HO volume in injured site from tenotomized Gli1-CreER T2 ; Acvr1 R206H/+ mice following vehicle and NF449 treatment ( n = 5 per group). **** P = 3.87e-6. ( Q , R ) Representative Safranine O staining images ( Q ) and statistical analysis ( R ) of Safranine O + region in injured site from tenotomized Gli1-CreER T2 ; Acvr1 R206H/+ and Gli1-CreER T2 ; Acvr1 R206H/+ ; Prkaca f/f mice at 7 dpi ( n = 5 per group). **** P = 6.2e-7. Scale bar, 100 μm. ( S , T ) Representative microCT images ( S ) and statistical analysis ( T ) of HO volume in injured site from tenotomized Gli1-CreER T2 ; Acvr1 R206H/+ and Gli1-CreER T2 ; Acvr1 R206H/+ ; Prkaca f/f mice at 14 dpi ( n = 5 per group). *** P = 1.79e-4. Data are presented as mean ± SD. All P values were determined by unpaired Student’s t test.

Article Snippet: Anti-mouse ACVR1 , Proteintech , Cat#67417-1-Ig.

Techniques: Immunofluorescence, Staining