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Servicebio Inc rabbit anti-rat collagen-1 antibody
Rabbit Anti Rat Collagen 1 Antibody, supplied by Servicebio Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/rabbit+anti-rat+collagen-1+antibody/collagen+i+rabbit+polyclonal+antibody/pmc09683673-54-23-27
Average 90 stars, based on 1 article reviews
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Incubation:

Article Title: Intact Fibroblast Growth Factor 23 Regulates Chronic Kidney Disease–Induced Myocardial Fibrosis by Activating the Sonic Hedgehog Signaling Pathway
Article Snippet: The paraffin sections were blocked with serum and incubated overnight with the following primary antibodies at 4 °C: rabbit anti‐rat Smoothened antibody (1:200; Affinity), rabbit anti‐rat Gli‐1 antibody (1:100; Novus), rabbit anti‐rat collagen‐1 antibody (1:1500; Servicebio), and rabbit anti‐rat collagen‐3 antibody (1:1000; Proteintech).

Article Title: Intact Fibroblast Growth Factor 23 Regulates Chronic Kidney Disease–Induced Myocardial Fibrosis by Activating the Sonic Hedgehog Signaling Pathway
Article Snippet: The following primary antibodies were added to the sections: rabbit anti‐rat Smoothened antibody (1:200; Affinity), rabbit anti‐rat Gli‐1 antibody (1:100; Novus, CO), rabbit anti‐rat collagen‐1 antibody (1:200; Servicebio), and rabbit anti‐rat collagen‐3 antibody (1:200; Proteintech, Wuhan, China).



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Figure 4 RCDs/UA@Lipo alleviated H2O2-induced oxidative stress and TGF-β1 induced fibrosis-specific markers separately. (A) Immunofluorescence staining images of intracellular ROS and superoxide detected by DCFH-DA probe. (B) mitochondrial membrane potential (ΔΨm) detected by JC-1 probe. (C) tendon fibrosis markers <t>(COL</t> I, COL <t>III,</t> α-SMA) of NIH3T3. (D–H) Semiquantitative analysis of the relative fluorescent intensity of (A–C) (n = 3). (D and E) Model group is H2O2 group, (F–H) Model group is TGF-β1 group. Data are presented as mean ± SD; comparisons between the groups were performed one-way ANOVA. *P < 0.05; **P < 0.01; ***P < 0.001.
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Figure 4 RCDs/UA@Lipo alleviated H2O2-induced oxidative stress and TGF-β1 induced fibrosis-specific markers separately. (A) Immunofluorescence staining images of intracellular ROS and superoxide detected by DCFH-DA probe. (B) mitochondrial membrane potential (ΔΨm) detected by JC-1 probe. (C) tendon fibrosis markers <t>(COL</t> I, COL <t>III,</t> α-SMA) of NIH3T3. (D–H) Semiquantitative analysis of the relative fluorescent intensity of (A–C) (n = 3). (D and E) Model group is H2O2 group, (F–H) Model group is TGF-β1 group. Data are presented as mean ± SD; comparisons between the groups were performed one-way ANOVA. *P < 0.05; **P < 0.01; ***P < 0.001.
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Figure 4 RCDs/UA@Lipo alleviated H2O2-induced oxidative stress and TGF-β1 induced fibrosis-specific markers separately. (A) Immunofluorescence staining images of intracellular ROS and superoxide detected by DCFH-DA probe. (B) mitochondrial membrane potential (ΔΨm) detected by JC-1 probe. (C) tendon fibrosis markers <t>(COL</t> I, COL <t>III,</t> α-SMA) of NIH3T3. (D–H) Semiquantitative analysis of the relative fluorescent intensity of (A–C) (n = 3). (D and E) Model group is H2O2 group, (F–H) Model group is TGF-β1 group. Data are presented as mean ± SD; comparisons between the groups were performed one-way ANOVA. *P < 0.05; **P < 0.01; ***P < 0.001.
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The images of H.E. staining and immunohistochemistry staining for prenatal rat dental germs. H.E. staining demonstrated that the rat dental germs entered the early cap stage at E14.5 d, the cap stage and early bell stage at E16.5 d, and the bell stage at E18.5 d. The separation between the pre-odontoblast and pre-ameloblast layers occurred in all E18.5 d species. Immunohistochemistry staining revealed that Clock , Per1 , and <t>Col1</t> were detected in the epithelial-mesenchymal interaction area, dental follicle, and dental papilla at E14.5 d, and became stronger at E16.5 d when p75NTR , Bmal1 , and ALP were detected. All the factors were expressed at E18.5 d, but Cry1 showed the weakest expression. All experiments were repeated three times independently. o p : oral epithelium; dp: dental papilla; iee: inner enamel epithelium; oee: outer enamel epithelium; sr: stellate reticulum. The scale bar represents 50 μm, respectively.
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The images of H.E. staining and immunohistochemistry staining for prenatal rat dental germs. H.E. staining demonstrated that the rat dental germs entered the early cap stage at E14.5 d, the cap stage and early bell stage at E16.5 d, and the bell stage at E18.5 d. The separation between the pre-odontoblast and pre-ameloblast layers occurred in all E18.5 d species. Immunohistochemistry staining revealed that Clock , Per1 , and <t>Col1</t> were detected in the epithelial-mesenchymal interaction area, dental follicle, and dental papilla at E14.5 d, and became stronger at E16.5 d when p75NTR , Bmal1 , and ALP were detected. All the factors were expressed at E18.5 d, but Cry1 showed the weakest expression. All experiments were repeated three times independently. o p : oral epithelium; dp: dental papilla; iee: inner enamel epithelium; oee: outer enamel epithelium; sr: stellate reticulum. The scale bar represents 50 μm, respectively.
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The images of H.E. staining and immunohistochemistry staining for prenatal rat dental germs. H.E. staining demonstrated that the rat dental germs entered the early cap stage at E14.5 d, the cap stage and early bell stage at E16.5 d, and the bell stage at E18.5 d. The separation between the pre-odontoblast and pre-ameloblast layers occurred in all E18.5 d species. Immunohistochemistry staining revealed that Clock , Per1 , and <t>Col1</t> were detected in the epithelial-mesenchymal interaction area, dental follicle, and dental papilla at E14.5 d, and became stronger at E16.5 d when p75NTR , Bmal1 , and ALP were detected. All the factors were expressed at E18.5 d, but Cry1 showed the weakest expression. All experiments were repeated three times independently. o p : oral epithelium; dp: dental papilla; iee: inner enamel epithelium; oee: outer enamel epithelium; sr: stellate reticulum. The scale bar represents 50 μm, respectively.
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The images of H.E. staining and immunohistochemistry staining for prenatal rat dental germs. H.E. staining demonstrated that the rat dental germs entered the early cap stage at E14.5 d, the cap stage and early bell stage at E16.5 d, and the bell stage at E18.5 d. The separation between the pre-odontoblast and pre-ameloblast layers occurred in all E18.5 d species. Immunohistochemistry staining revealed that Clock , Per1 , and <t>Col1</t> were detected in the epithelial-mesenchymal interaction area, dental follicle, and dental papilla at E14.5 d, and became stronger at E16.5 d when p75NTR , Bmal1 , and ALP were detected. All the factors were expressed at E18.5 d, but Cry1 showed the weakest expression. All experiments were repeated three times independently. o p : oral epithelium; dp: dental papilla; iee: inner enamel epithelium; oee: outer enamel epithelium; sr: stellate reticulum. The scale bar represents 50 μm, respectively.
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Image Search Results


Figure 4 RCDs/UA@Lipo alleviated H2O2-induced oxidative stress and TGF-β1 induced fibrosis-specific markers separately. (A) Immunofluorescence staining images of intracellular ROS and superoxide detected by DCFH-DA probe. (B) mitochondrial membrane potential (ΔΨm) detected by JC-1 probe. (C) tendon fibrosis markers (COL I, COL III, α-SMA) of NIH3T3. (D–H) Semiquantitative analysis of the relative fluorescent intensity of (A–C) (n = 3). (D and E) Model group is H2O2 group, (F–H) Model group is TGF-β1 group. Data are presented as mean ± SD; comparisons between the groups were performed one-way ANOVA. *P < 0.05; **P < 0.01; ***P < 0.001.

Journal: International Journal of Nanomedicine

Article Title: Antioxidant Carbon Dots and Ursolic Acid Co-Encapsulated Liposomes Composite Hydrogel for Alleviating Adhesion Formation and Enhancing Tendon Healing in Tendon Injury

doi: 10.2147/ijn.s466312

Figure Lengend Snippet: Figure 4 RCDs/UA@Lipo alleviated H2O2-induced oxidative stress and TGF-β1 induced fibrosis-specific markers separately. (A) Immunofluorescence staining images of intracellular ROS and superoxide detected by DCFH-DA probe. (B) mitochondrial membrane potential (ΔΨm) detected by JC-1 probe. (C) tendon fibrosis markers (COL I, COL III, α-SMA) of NIH3T3. (D–H) Semiquantitative analysis of the relative fluorescent intensity of (A–C) (n = 3). (D and E) Model group is H2O2 group, (F–H) Model group is TGF-β1 group. Data are presented as mean ± SD; comparisons between the groups were performed one-way ANOVA. *P < 0.05; **P < 0.01; ***P < 0.001.

Article Snippet: Evaluation of Anti-Fibrotic Effects of the Biomaterials by Immunofluorescent Staining at Six Weeks The fresh tissue sections were incubated with rabbit anti-rat antibodies against COL III (1:200; Cat#22734-1-AP, Proteintech, USA) and α-SMA (1:200; Cat#19245S, Cell Signaling Technology, USA) at 4°C overnight.

Techniques: Immunofluorescence, Staining, Membrane

Figure 6 RCDs/UA@Lipo-HAMA reduced adhesion of injured tendons at macroscopic and histological levels at various time points post-injury. (A) Schematic diagram of surgical procedures of the ATI. (B) Gross view of ATI. (C)Representative images of immunofluorescence staining of tendon antioxidant (Nrf-2, HO-1) and anti-inflammatory markers (CD68, iNOS) at 2 weeks post-injury (n = 3). (D) Representative images of immunofluorescence staining of tendon antifibrosis (COL III, α-SMA) at 6 weeks post- injury (n = 3). (E) Representative images of immunohistochemical staining of tendon markers (Vimentin, MMP2, α-SMA) antifibrosis at 6 weeks post-injury (n = 4). (F–N) Semiquantitative analysis of expression level of tendon marker of (C–E), respectively. Data are presented as mean ± SD; comparisons between the groups were performed by one-way ANOVA. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001.

Journal: International Journal of Nanomedicine

Article Title: Antioxidant Carbon Dots and Ursolic Acid Co-Encapsulated Liposomes Composite Hydrogel for Alleviating Adhesion Formation and Enhancing Tendon Healing in Tendon Injury

doi: 10.2147/ijn.s466312

Figure Lengend Snippet: Figure 6 RCDs/UA@Lipo-HAMA reduced adhesion of injured tendons at macroscopic and histological levels at various time points post-injury. (A) Schematic diagram of surgical procedures of the ATI. (B) Gross view of ATI. (C)Representative images of immunofluorescence staining of tendon antioxidant (Nrf-2, HO-1) and anti-inflammatory markers (CD68, iNOS) at 2 weeks post-injury (n = 3). (D) Representative images of immunofluorescence staining of tendon antifibrosis (COL III, α-SMA) at 6 weeks post- injury (n = 3). (E) Representative images of immunohistochemical staining of tendon markers (Vimentin, MMP2, α-SMA) antifibrosis at 6 weeks post-injury (n = 4). (F–N) Semiquantitative analysis of expression level of tendon marker of (C–E), respectively. Data are presented as mean ± SD; comparisons between the groups were performed by one-way ANOVA. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001.

Article Snippet: Evaluation of Anti-Fibrotic Effects of the Biomaterials by Immunofluorescent Staining at Six Weeks The fresh tissue sections were incubated with rabbit anti-rat antibodies against COL III (1:200; Cat#22734-1-AP, Proteintech, USA) and α-SMA (1:200; Cat#19245S, Cell Signaling Technology, USA) at 4°C overnight.

Techniques: Immunofluorescence, Staining, Immunohistochemical staining, Expressing, Marker

The images of H.E. staining and immunohistochemistry staining for prenatal rat dental germs. H.E. staining demonstrated that the rat dental germs entered the early cap stage at E14.5 d, the cap stage and early bell stage at E16.5 d, and the bell stage at E18.5 d. The separation between the pre-odontoblast and pre-ameloblast layers occurred in all E18.5 d species. Immunohistochemistry staining revealed that Clock , Per1 , and Col1 were detected in the epithelial-mesenchymal interaction area, dental follicle, and dental papilla at E14.5 d, and became stronger at E16.5 d when p75NTR , Bmal1 , and ALP were detected. All the factors were expressed at E18.5 d, but Cry1 showed the weakest expression. All experiments were repeated three times independently. o p : oral epithelium; dp: dental papilla; iee: inner enamel epithelium; oee: outer enamel epithelium; sr: stellate reticulum. The scale bar represents 50 μm, respectively.

Journal: Frontiers in Physiology

Article Title: A potential role of p75NTR in the regulation of circadian rhythm and incremental growth lines during tooth development

doi: 10.3389/fphys.2022.981311

Figure Lengend Snippet: The images of H.E. staining and immunohistochemistry staining for prenatal rat dental germs. H.E. staining demonstrated that the rat dental germs entered the early cap stage at E14.5 d, the cap stage and early bell stage at E16.5 d, and the bell stage at E18.5 d. The separation between the pre-odontoblast and pre-ameloblast layers occurred in all E18.5 d species. Immunohistochemistry staining revealed that Clock , Per1 , and Col1 were detected in the epithelial-mesenchymal interaction area, dental follicle, and dental papilla at E14.5 d, and became stronger at E16.5 d when p75NTR , Bmal1 , and ALP were detected. All the factors were expressed at E18.5 d, but Cry1 showed the weakest expression. All experiments were repeated three times independently. o p : oral epithelium; dp: dental papilla; iee: inner enamel epithelium; oee: outer enamel epithelium; sr: stellate reticulum. The scale bar represents 50 μm, respectively.

Article Snippet: The primary antibodies were used in this study are as follows: rabbit anti-rat p75NTR (1:1,500; Abcam, Cambridge, MA, United States, ab245134, monoclonal), rabbit anti-rat BMAL1 (1:1,000; Abcam, Cambridge, MA, United States, ab230822, monoclonal), rabbit anti-rat CLOCK (1:1,000; Abcam, Cambridge, MA, United States, ab3517, polyclonal), rabbit anti-rat PER1 (1:500; Bioss, Beijing, China,bs-2350R, polyclonal), rabbit anti-rat CRY1 (1:500; Bioss, Beijing, China bs-11441R, polyclonal), rabbit anti-rat ALP (1:500; Bioss, Beijing, China, bs-2928R, polyclonal), rabbit anti-rat COL1 (1:500; Bioss, Beijing, China, bs-0578R, polyclonal).

Techniques: Staining, Immunohistochemistry, Expressing

Mice oligonucleotide primers used in this study.

Journal: Frontiers in Physiology

Article Title: A potential role of p75NTR in the regulation of circadian rhythm and incremental growth lines during tooth development

doi: 10.3389/fphys.2022.981311

Figure Lengend Snippet: Mice oligonucleotide primers used in this study.

Article Snippet: The primary antibodies were used in this study are as follows: rabbit anti-rat p75NTR (1:1,500; Abcam, Cambridge, MA, United States, ab245134, monoclonal), rabbit anti-rat BMAL1 (1:1,000; Abcam, Cambridge, MA, United States, ab230822, monoclonal), rabbit anti-rat CLOCK (1:1,000; Abcam, Cambridge, MA, United States, ab3517, polyclonal), rabbit anti-rat PER1 (1:500; Bioss, Beijing, China,bs-2350R, polyclonal), rabbit anti-rat CRY1 (1:500; Bioss, Beijing, China bs-11441R, polyclonal), rabbit anti-rat ALP (1:500; Bioss, Beijing, China, bs-2928R, polyclonal), rabbit anti-rat COL1 (1:500; Bioss, Beijing, China, bs-0578R, polyclonal).

Techniques:

The in vivo observation of circadian rhythm dynamics in PN7 d dental germs of wild-type mice. p75NTR mRNA showed a significant difference between D.D. and L.D. conditions ( p < 0.05), but the change tendencies at two sampling times were opposite: p75NTR mRNA expression in the L.D. condition was significantly higher at 7:30 a.m. and significantly lower at 7:30 p.m. in the D.D. condition ( p < 0.05). The expression pattern of Mage-D1 was similar to that of p75NTR. Most factors ( Bmal1 , Clock , Per1 , Per2 , Runx2 , ALP , Col1 , and Dlx1 ) showed the same change tendency at the two sampling times: mRNA expression was significantly higher in the D.D. condition than that in the L.D. condition ( p < 0.05). The change amplitudes of Clock , Per1 , Per2 , Runx2 , and Dlx1 were significantly larger at the sampling time of 7:30 PM. Contrary to p75NTR , Msx1 mRNA expression in the L.D. condition was significantly lower at 7:30 a.m. and significantly higher at 7:30 p.m. compared with the D.D. condition ( p < 0.05). Dmp1 and Dspp mRNA expression in the D.D. condition was significantly lower than that in L.D. condition at both sampling times ( p < 0.05). All experiments were repeated at least three times independently. Data are expressed as mean ± S.D. L. D. Condition group, n = 11; D. D. Condition group, n = 5.

Journal: Frontiers in Physiology

Article Title: A potential role of p75NTR in the regulation of circadian rhythm and incremental growth lines during tooth development

doi: 10.3389/fphys.2022.981311

Figure Lengend Snippet: The in vivo observation of circadian rhythm dynamics in PN7 d dental germs of wild-type mice. p75NTR mRNA showed a significant difference between D.D. and L.D. conditions ( p < 0.05), but the change tendencies at two sampling times were opposite: p75NTR mRNA expression in the L.D. condition was significantly higher at 7:30 a.m. and significantly lower at 7:30 p.m. in the D.D. condition ( p < 0.05). The expression pattern of Mage-D1 was similar to that of p75NTR. Most factors ( Bmal1 , Clock , Per1 , Per2 , Runx2 , ALP , Col1 , and Dlx1 ) showed the same change tendency at the two sampling times: mRNA expression was significantly higher in the D.D. condition than that in the L.D. condition ( p < 0.05). The change amplitudes of Clock , Per1 , Per2 , Runx2 , and Dlx1 were significantly larger at the sampling time of 7:30 PM. Contrary to p75NTR , Msx1 mRNA expression in the L.D. condition was significantly lower at 7:30 a.m. and significantly higher at 7:30 p.m. compared with the D.D. condition ( p < 0.05). Dmp1 and Dspp mRNA expression in the D.D. condition was significantly lower than that in L.D. condition at both sampling times ( p < 0.05). All experiments were repeated at least three times independently. Data are expressed as mean ± S.D. L. D. Condition group, n = 11; D. D. Condition group, n = 5.

Article Snippet: The primary antibodies were used in this study are as follows: rabbit anti-rat p75NTR (1:1,500; Abcam, Cambridge, MA, United States, ab245134, monoclonal), rabbit anti-rat BMAL1 (1:1,000; Abcam, Cambridge, MA, United States, ab230822, monoclonal), rabbit anti-rat CLOCK (1:1,000; Abcam, Cambridge, MA, United States, ab3517, polyclonal), rabbit anti-rat PER1 (1:500; Bioss, Beijing, China,bs-2350R, polyclonal), rabbit anti-rat CRY1 (1:500; Bioss, Beijing, China bs-11441R, polyclonal), rabbit anti-rat ALP (1:500; Bioss, Beijing, China, bs-2928R, polyclonal), rabbit anti-rat COL1 (1:500; Bioss, Beijing, China, bs-0578R, polyclonal).

Techniques: In Vivo, Sampling, Expressing

The in vivo assays for the effect of p75NTR knockout on the mRNA expression in dental germs at PN7d. As expected, p75NTR mRNA in the knockout mice was significantly lower than in THE wild-type mice ( p < 0.05). Mage-D1 , Bmal1 , ALP , Col1 , Msx1 , Dmp1 , and Dspp showed the same change in the p75NTR knockout mice, indicating a positive relationship with p75NTR . In contrast, Runx2 showed the reverse change, presenting a negative relationship with p75NTR . Clock , Per1 , Per2 , and Dlx1 showed no significant difference between p75NTR knockout and wild-type mice ( p > 0.05). All experiments were repeated at least three times independently. Data are expressed as mean ± S.D. L. D. Condition group, n = 6; D. D. Condition group, n = 6.

Journal: Frontiers in Physiology

Article Title: A potential role of p75NTR in the regulation of circadian rhythm and incremental growth lines during tooth development

doi: 10.3389/fphys.2022.981311

Figure Lengend Snippet: The in vivo assays for the effect of p75NTR knockout on the mRNA expression in dental germs at PN7d. As expected, p75NTR mRNA in the knockout mice was significantly lower than in THE wild-type mice ( p < 0.05). Mage-D1 , Bmal1 , ALP , Col1 , Msx1 , Dmp1 , and Dspp showed the same change in the p75NTR knockout mice, indicating a positive relationship with p75NTR . In contrast, Runx2 showed the reverse change, presenting a negative relationship with p75NTR . Clock , Per1 , Per2 , and Dlx1 showed no significant difference between p75NTR knockout and wild-type mice ( p > 0.05). All experiments were repeated at least three times independently. Data are expressed as mean ± S.D. L. D. Condition group, n = 6; D. D. Condition group, n = 6.

Article Snippet: The primary antibodies were used in this study are as follows: rabbit anti-rat p75NTR (1:1,500; Abcam, Cambridge, MA, United States, ab245134, monoclonal), rabbit anti-rat BMAL1 (1:1,000; Abcam, Cambridge, MA, United States, ab230822, monoclonal), rabbit anti-rat CLOCK (1:1,000; Abcam, Cambridge, MA, United States, ab3517, polyclonal), rabbit anti-rat PER1 (1:500; Bioss, Beijing, China,bs-2350R, polyclonal), rabbit anti-rat CRY1 (1:500; Bioss, Beijing, China bs-11441R, polyclonal), rabbit anti-rat ALP (1:500; Bioss, Beijing, China, bs-2928R, polyclonal), rabbit anti-rat COL1 (1:500; Bioss, Beijing, China, bs-0578R, polyclonal).

Techniques: In Vivo, Knock-Out, Expressing

The in vitro assays for the effect of p75NTR over-expression on the mRNA expression in immortalizing stem cells from dental apical papilla (iSCAP). p75NTR was expected to be significantly higher expressed in the over-expression group than that in the control group ( p < 0.05). Mage-D1 , Bmal1 , Clock , Runx2 , Col1 , and Msx1 showed an apparent positive relationship when p75NTR was significantly up-regulated. In contrast, ALP , Dmp1 , and Dspp showed a negative relationship with p75NTR . Per1 , Per2 , ALP , Dlx1 , and Dmp1 showed no significant difference between the over-expression group and control group ( p > 0.05) with lower than that in wild-type mice ( p < 0.05). All experiments were repeated at least three times independently. Data are expressed as mean ± S.D. Overexpression negative control group, n = 3; p75NTR over-expression group, n = 3.

Journal: Frontiers in Physiology

Article Title: A potential role of p75NTR in the regulation of circadian rhythm and incremental growth lines during tooth development

doi: 10.3389/fphys.2022.981311

Figure Lengend Snippet: The in vitro assays for the effect of p75NTR over-expression on the mRNA expression in immortalizing stem cells from dental apical papilla (iSCAP). p75NTR was expected to be significantly higher expressed in the over-expression group than that in the control group ( p < 0.05). Mage-D1 , Bmal1 , Clock , Runx2 , Col1 , and Msx1 showed an apparent positive relationship when p75NTR was significantly up-regulated. In contrast, ALP , Dmp1 , and Dspp showed a negative relationship with p75NTR . Per1 , Per2 , ALP , Dlx1 , and Dmp1 showed no significant difference between the over-expression group and control group ( p > 0.05) with lower than that in wild-type mice ( p < 0.05). All experiments were repeated at least three times independently. Data are expressed as mean ± S.D. Overexpression negative control group, n = 3; p75NTR over-expression group, n = 3.

Article Snippet: The primary antibodies were used in this study are as follows: rabbit anti-rat p75NTR (1:1,500; Abcam, Cambridge, MA, United States, ab245134, monoclonal), rabbit anti-rat BMAL1 (1:1,000; Abcam, Cambridge, MA, United States, ab230822, monoclonal), rabbit anti-rat CLOCK (1:1,000; Abcam, Cambridge, MA, United States, ab3517, polyclonal), rabbit anti-rat PER1 (1:500; Bioss, Beijing, China,bs-2350R, polyclonal), rabbit anti-rat CRY1 (1:500; Bioss, Beijing, China bs-11441R, polyclonal), rabbit anti-rat ALP (1:500; Bioss, Beijing, China, bs-2928R, polyclonal), rabbit anti-rat COL1 (1:500; Bioss, Beijing, China, bs-0578R, polyclonal).

Techniques: In Vitro, Over Expression, Expressing, Negative Control