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R&D Systems recombinant wnt5b protein
Recombinant Wnt5b Protein, supplied by R&D Systems, 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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Figure 1. SNP rs2887571 correlates with WNT5B expression in primary human osteoblasts (A) Nucleotide sequence near SNP rs2887571 with predicted NFAT and ERa binding motifs. (B) Diagram representing the location between SNP rs2887571 and nearby genes in chromosome 12. (C–G) Expression of (C) ERC1, (D) LINC00942, (E) LOC107984507, (F) FBXL14, and (G) WNT5B were measured by qPCR and compared with its genotype for SNP rs2887571 in human osteoblasts (AA ¼ 52, AG ¼ 49, and GG ¼ 9). Bars indicate median with interquartile range. Mann-Whitney U-test: **p ¼ 0.0016.

Journal: American journal of human genetics

Article Title: Estrogen receptor alpha and NFATc1 bind to a bone mineral density-associated SNP to repress WNT5B in osteoblasts.

doi: 10.1016/j.ajhg.2021.11.018

Figure Lengend Snippet: Figure 1. SNP rs2887571 correlates with WNT5B expression in primary human osteoblasts (A) Nucleotide sequence near SNP rs2887571 with predicted NFAT and ERa binding motifs. (B) Diagram representing the location between SNP rs2887571 and nearby genes in chromosome 12. (C–G) Expression of (C) ERC1, (D) LINC00942, (E) LOC107984507, (F) FBXL14, and (G) WNT5B were measured by qPCR and compared with its genotype for SNP rs2887571 in human osteoblasts (AA ¼ 52, AG ¼ 49, and GG ¼ 9). Bars indicate median with interquartile range. Mann-Whitney U-test: **p ¼ 0.0016.

Article Snippet: Recombinant mouse WNT5B (rWNT5B; Cat. # 3006-WN) was acquired from R&D Systems.

Techniques: Expressing, Sequencing, Binding Assay, MANN-WHITNEY

Figure 2. E2 suppresses WNT5B expres- sion via ERa (A–D) Human osteoblasts (hOBs) and oste- oblast-like U2OS-ERa cells were treated with EtOH or 10 nM E2 for 4 h then levels of (A, C) WNT5B mRNA expression were detected by qPCR. Immunoblotting anal- ysis of WNT5B protein expression after treatment with EtOH or 10 nM E2 for 24 h and normalized to b-actin (BA) and quantiﬁed by ImageJ in (B) hOBs and (D) U2OS-ERa cells. Bar ¼ mean with SEM. n ¼ 3, Student’s t test: *p<0.05. Three different biological replicates of hOBs and U2OS-ERa cells were tested and a represen- tative picture from one biological replicate is presented. (E) Mouse osteoblasts (mOBs) were differ- entiated for 3 and 7 days then treated with EtOH or 10 nM E2 for 24 h, and levels of Wnt5b mRNA expression were detected by qPCR. The level of WNT5B was detected by IHC in mice from sham-treated, ovariec- tomized (OVX), and OVX then treated with E2. (F) The number of WNT5B-positive osteo- blasts were counted and divided by the to- tal osteoblasts from three different mice in each group. Bar ¼ mean with SEM. n ¼ 3, Student’s t test: ****p < 0.0001, **p < 0.01, *p < 0.05. (G) The regions of interest (red square) are shown below at 403 magniﬁcation. Black scale bar ¼ 200 mM, red scale bar ¼ 20 mM, red arrow ¼ osteoblast, and asterisk ¼ osteoid.

Journal: American journal of human genetics

Article Title: Estrogen receptor alpha and NFATc1 bind to a bone mineral density-associated SNP to repress WNT5B in osteoblasts.

doi: 10.1016/j.ajhg.2021.11.018

Figure Lengend Snippet: Figure 2. E2 suppresses WNT5B expres- sion via ERa (A–D) Human osteoblasts (hOBs) and oste- oblast-like U2OS-ERa cells were treated with EtOH or 10 nM E2 for 4 h then levels of (A, C) WNT5B mRNA expression were detected by qPCR. Immunoblotting anal- ysis of WNT5B protein expression after treatment with EtOH or 10 nM E2 for 24 h and normalized to b-actin (BA) and quantiﬁed by ImageJ in (B) hOBs and (D) U2OS-ERa cells. Bar ¼ mean with SEM. n ¼ 3, Student’s t test: *p<0.05. Three different biological replicates of hOBs and U2OS-ERa cells were tested and a represen- tative picture from one biological replicate is presented. (E) Mouse osteoblasts (mOBs) were differ- entiated for 3 and 7 days then treated with EtOH or 10 nM E2 for 24 h, and levels of Wnt5b mRNA expression were detected by qPCR. The level of WNT5B was detected by IHC in mice from sham-treated, ovariec- tomized (OVX), and OVX then treated with E2. (F) The number of WNT5B-positive osteo- blasts were counted and divided by the to- tal osteoblasts from three different mice in each group. Bar ¼ mean with SEM. n ¼ 3, Student’s t test: ****p < 0.0001, **p < 0.01, *p < 0.05. (G) The regions of interest (red square) are shown below at 403 magniﬁcation. Black scale bar ¼ 200 mM, red scale bar ¼ 20 mM, red arrow ¼ osteoblast, and asterisk ¼ osteoid.

Article Snippet: Recombinant mouse WNT5B (rWNT5B; Cat. # 3006-WN) was acquired from R&D Systems.

Techniques: Expressing, Western Blot

Figure 3. ERa and NFATc1 interact and bind at SNP rs2887571 (A–D) U2OS-ERa cells were treated with or without 10 nM E2 for 45 min, then ChIP was performed using an antibody to (A) ERa, (B) H3K27ac, (C) SIN3A, or (D) NFATc1. qPCR was performed with primers for SNP rs2887571 in comparison with b-actin (ACTB) promoter or hemoglobin (HBB) promoter. (E) U2OS-ERa cells were treated with 10 nM E2, then ChIP-reChIP was performed with antibodies to ERa, NFATc1 and/or IgG, and primers for SNP rs2887571. (F) Human genomic DNA around SNP rs2887571 was ampliﬁed and inserted into the pGL3 vector, then U2OS-ERa cells were transfected with pGL3-rs2887571, in the presence or absence of EGFPC1-huNFATc1EE-WT. Cells were treated with Dox. to induce ERa. 24 h later, cells were treated with EtOH or 10 nM E2 for an additional 24 h. Relative luciferase activity was measured using dual-luciferase reporter assays. (G) U2OS-ERa cells were transfected with pGL3-rs2887571 and EGFPC1-huNFATc1EE-WT, together with or without pCS2þMT-mSin3A, before being induced or uninduced to express ERa. Cells were treated with EtOH or 10 nM E2 and the relative luciferase activity was detected at 24 h. Luciferase activity was normalized with pRL-SV40 (Renilla). (H and I) U2OS-ERa cells were transfected with siRNA directed against SIN3A mRNA, before being treated with or without 10 nM E2. The mRNA levels of (H) SIN3A and (I) WNT5B were detected by qPCR. n ¼ 3, Student’s t test: ****p < 0.0001, ***p < 0.001, **p < 0.01, *p < 0.05.

Journal: American journal of human genetics

Article Title: Estrogen receptor alpha and NFATc1 bind to a bone mineral density-associated SNP to repress WNT5B in osteoblasts.

doi: 10.1016/j.ajhg.2021.11.018

Figure Lengend Snippet: Figure 3. ERa and NFATc1 interact and bind at SNP rs2887571 (A–D) U2OS-ERa cells were treated with or without 10 nM E2 for 45 min, then ChIP was performed using an antibody to (A) ERa, (B) H3K27ac, (C) SIN3A, or (D) NFATc1. qPCR was performed with primers for SNP rs2887571 in comparison with b-actin (ACTB) promoter or hemoglobin (HBB) promoter. (E) U2OS-ERa cells were treated with 10 nM E2, then ChIP-reChIP was performed with antibodies to ERa, NFATc1 and/or IgG, and primers for SNP rs2887571. (F) Human genomic DNA around SNP rs2887571 was ampliﬁed and inserted into the pGL3 vector, then U2OS-ERa cells were transfected with pGL3-rs2887571, in the presence or absence of EGFPC1-huNFATc1EE-WT. Cells were treated with Dox. to induce ERa. 24 h later, cells were treated with EtOH or 10 nM E2 for an additional 24 h. Relative luciferase activity was measured using dual-luciferase reporter assays. (G) U2OS-ERa cells were transfected with pGL3-rs2887571 and EGFPC1-huNFATc1EE-WT, together with or without pCS2þMT-mSin3A, before being induced or uninduced to express ERa. Cells were treated with EtOH or 10 nM E2 and the relative luciferase activity was detected at 24 h. Luciferase activity was normalized with pRL-SV40 (Renilla). (H and I) U2OS-ERa cells were transfected with siRNA directed against SIN3A mRNA, before being treated with or without 10 nM E2. The mRNA levels of (H) SIN3A and (I) WNT5B were detected by qPCR. n ¼ 3, Student’s t test: ****p < 0.0001, ***p < 0.001, **p < 0.01, *p < 0.05.

Article Snippet: Recombinant mouse WNT5B (rWNT5B; Cat. # 3006-WN) was acquired from R&D Systems.

Techniques: Comparison, Plasmid Preparation, Transfection, Luciferase, Activity Assay

Figure 4. SNP rs2887571 has allelic spec- iﬁcities to alter WNT5B expression (A) U2OS-ERa cells with either homozy- gous AA and GG at SNP rs2887571 were lysed and immunoblotting was performed with an antibody to WNT5B. The level of protein was normalized with b-actin and quantiﬁed by ImageJ. Bar ¼ mean with SEM. n ¼ 3, Student’s t test: *p < 0.05. (B–D) Three different biological replicates of U2OS-ERa cells were tested and a repre- sentative picture from one biological repli- cate is presented. ChIP was performed us- ing an antibody to (B) ERa, (C) SIN3A and (D) NFATc1, and qPCR was done with primers for SNP rs2887571 in compar- ison with the ACTB promoter. n ¼ 3, Stu- dent’s t test: **p < 0.01, *p < 0.05.

Journal: American journal of human genetics

Article Title: Estrogen receptor alpha and NFATc1 bind to a bone mineral density-associated SNP to repress WNT5B in osteoblasts.

doi: 10.1016/j.ajhg.2021.11.018

Figure Lengend Snippet: Figure 4. SNP rs2887571 has allelic spec- iﬁcities to alter WNT5B expression (A) U2OS-ERa cells with either homozy- gous AA and GG at SNP rs2887571 were lysed and immunoblotting was performed with an antibody to WNT5B. The level of protein was normalized with b-actin and quantiﬁed by ImageJ. Bar ¼ mean with SEM. n ¼ 3, Student’s t test: *p < 0.05. (B–D) Three different biological replicates of U2OS-ERa cells were tested and a repre- sentative picture from one biological repli- cate is presented. ChIP was performed us- ing an antibody to (B) ERa, (C) SIN3A and (D) NFATc1, and qPCR was done with primers for SNP rs2887571 in compar- ison with the ACTB promoter. n ¼ 3, Stu- dent’s t test: **p < 0.01, *p < 0.05.

Article Snippet: Recombinant mouse WNT5B (rWNT5B; Cat. # 3006-WN) was acquired from R&D Systems.

Techniques: Expressing, Western Blot

Figure 5. WNT5B suppresses osteoblast differentiation and promotes adipogenesis (A–C) mOBs were isolated from calvaria then treated with various doses of rWNT5B at day 0 (D0), day 7 after differentiation (D7) or day 14 after differentiation (D14) for 24 h. The levels of (A) Sp7, (B) Alpl, and (C) Bglap were detected by qPCR. (D) mOBs were treated with or without 50 ng/mL rWNT5B and stained for alkaline phosphatase (ALP) and Alizarin Red. (E) The levels of Alizarin Red in Ctrl and WNT5B groups were quantiﬁed at O.D. 570 nm and shown as % of the control. (F) mOBs were infected with lentivirus containing sh-Ctrl or sh-Wnt5b, before collecting mRNA or protein. The levels of WNT5B mRNA and protein were normalized with b-actin and quantiﬁed by ImageJ. (G and H) Cells were differentiated for 7 days in the presence or absence of 50 ng/mL rWNT5B, then (G) expression of Bglap was detected by qPCR and (H) alkaline phosphatase (ALP) activity was detected at O.D. 405 nm then was normalized with total protein. (I) Bone marrow-derived MSCs were treated with or without 50 ng/mL rWNT5B in osteogenic differentiation media for 12 days and stained with Alizarin Red. CFU-OB was reported as the number of colonies. (J) Bone marrow-derived MSCs were treated with or without 50 ng/mL rWNT5B in adipogenic differentiation medium for 14 days and stained with Oil Red O. (K) The levels of Oil Red O between Ctrl and WNT5B groups were quantiﬁed as % Area by ImageJ. (L and M) Expression of (L) Pparg and (M) Adipoq in MSC-derived adipocytes treated with or without rWNT5B for 24 h were detected by qPCR. Three different biological replicates were obtained and a representative image or graph from one replicate is presented. n ¼ 3, Student’s t test: ****p < 0.0001, ***p < 0.001, **p < 0.01, *p < 0.05.

Journal: American journal of human genetics

Article Title: Estrogen receptor alpha and NFATc1 bind to a bone mineral density-associated SNP to repress WNT5B in osteoblasts.

doi: 10.1016/j.ajhg.2021.11.018

Figure Lengend Snippet: Figure 5. WNT5B suppresses osteoblast differentiation and promotes adipogenesis (A–C) mOBs were isolated from calvaria then treated with various doses of rWNT5B at day 0 (D0), day 7 after differentiation (D7) or day 14 after differentiation (D14) for 24 h. The levels of (A) Sp7, (B) Alpl, and (C) Bglap were detected by qPCR. (D) mOBs were treated with or without 50 ng/mL rWNT5B and stained for alkaline phosphatase (ALP) and Alizarin Red. (E) The levels of Alizarin Red in Ctrl and WNT5B groups were quantiﬁed at O.D. 570 nm and shown as % of the control. (F) mOBs were infected with lentivirus containing sh-Ctrl or sh-Wnt5b, before collecting mRNA or protein. The levels of WNT5B mRNA and protein were normalized with b-actin and quantiﬁed by ImageJ. (G and H) Cells were differentiated for 7 days in the presence or absence of 50 ng/mL rWNT5B, then (G) expression of Bglap was detected by qPCR and (H) alkaline phosphatase (ALP) activity was detected at O.D. 405 nm then was normalized with total protein. (I) Bone marrow-derived MSCs were treated with or without 50 ng/mL rWNT5B in osteogenic differentiation media for 12 days and stained with Alizarin Red. CFU-OB was reported as the number of colonies. (J) Bone marrow-derived MSCs were treated with or without 50 ng/mL rWNT5B in adipogenic differentiation medium for 14 days and stained with Oil Red O. (K) The levels of Oil Red O between Ctrl and WNT5B groups were quantiﬁed as % Area by ImageJ. (L and M) Expression of (L) Pparg and (M) Adipoq in MSC-derived adipocytes treated with or without rWNT5B for 24 h were detected by qPCR. Three different biological replicates were obtained and a representative image or graph from one replicate is presented. n ¼ 3, Student’s t test: ****p < 0.0001, ***p < 0.001, **p < 0.01, *p < 0.05.

Article Snippet: Recombinant mouse WNT5B (rWNT5B; Cat. # 3006-WN) was acquired from R&D Systems.

Techniques: Isolation, Staining, Control, Infection, Expressing, Activity Assay, Derivative Assay

Figure 6. WNT5B activates WNT-PCP signaling pathway via ROR1/2 and inhibits b-catenin activity in osteoblasts (A) U2OS-ERa cells were transfected with Super8XTOPFlash (a luciferase reporter for b-catenin activity) together with empty vector (pcDNA3), WNT5B, WNT10B, or WNT5B with WNT10B vectors. After 48 h, relative luciferase activity was measured using dual-luciferase reporter assays. Fireﬂy luciferase activity was normalized to pRL-SV40 (Renilla). (B) mOBs were differentiated for 7 days before treatment with or without 50 ng/mL rWNT5B for 30 min and the levels of active b-catenin (ABC) was detected by immunoﬂuorescence. Scale bar ¼ 10 mM. Three different mOBs were tested in biological replicates and a repre- sentative image from one replicate is presented. (C) Differentiated mOBs at D7 were treated with 50 ng/mL rWNT5B and total cell lysate was collected at different time points before detecting the level of phospho-b-catenin (Ser552), ABC, total b-catenin, and b-actin by immunoblotting. (D and E) mOBs were differentiated for 7 days before treatment with or without 50 ng/mL rWNT5B for 30 min and localization of WNT5B with (D) ROR1 or (E) ROR2 were detected by immunoﬂuorescence. Scale bar ¼ 10 mM. (F and G) mOBs were differentiated for 7 days and treated with 50 ng/mL rWNT5B, and protein was collected at 0, 15, 30, and 60 min. The levels of downstream effectors were detected with the indicated antibodies. (H–J) mOBs (H), MSCs (I), and MSC-derived adipocytes (J) were treated with or without 50 ng/mL rWNT5B for 24 h and qPCR was per- formed for Il6 mRNA. (K) mOBs were treated with 50 ng/mL rWNT5B for 1 h and then ChIP was performed using a speciﬁc antibody to phospho-c-Fos (Ser32) and qPCR using primers to mouse negative control binding site and the Il6 promoter. n ¼ 3, Student’s t test: ****p < 0.0001, **p < 0.01, *p < 0.05.

Journal: American journal of human genetics

Article Title: Estrogen receptor alpha and NFATc1 bind to a bone mineral density-associated SNP to repress WNT5B in osteoblasts.

doi: 10.1016/j.ajhg.2021.11.018

Figure Lengend Snippet: Figure 6. WNT5B activates WNT-PCP signaling pathway via ROR1/2 and inhibits b-catenin activity in osteoblasts (A) U2OS-ERa cells were transfected with Super8XTOPFlash (a luciferase reporter for b-catenin activity) together with empty vector (pcDNA3), WNT5B, WNT10B, or WNT5B with WNT10B vectors. After 48 h, relative luciferase activity was measured using dual-luciferase reporter assays. Fireﬂy luciferase activity was normalized to pRL-SV40 (Renilla). (B) mOBs were differentiated for 7 days before treatment with or without 50 ng/mL rWNT5B for 30 min and the levels of active b-catenin (ABC) was detected by immunoﬂuorescence. Scale bar ¼ 10 mM. Three different mOBs were tested in biological replicates and a repre- sentative image from one replicate is presented. (C) Differentiated mOBs at D7 were treated with 50 ng/mL rWNT5B and total cell lysate was collected at different time points before detecting the level of phospho-b-catenin (Ser552), ABC, total b-catenin, and b-actin by immunoblotting. (D and E) mOBs were differentiated for 7 days before treatment with or without 50 ng/mL rWNT5B for 30 min and localization of WNT5B with (D) ROR1 or (E) ROR2 were detected by immunoﬂuorescence. Scale bar ¼ 10 mM. (F and G) mOBs were differentiated for 7 days and treated with 50 ng/mL rWNT5B, and protein was collected at 0, 15, 30, and 60 min. The levels of downstream effectors were detected with the indicated antibodies. (H–J) mOBs (H), MSCs (I), and MSC-derived adipocytes (J) were treated with or without 50 ng/mL rWNT5B for 24 h and qPCR was per- formed for Il6 mRNA. (K) mOBs were treated with 50 ng/mL rWNT5B for 1 h and then ChIP was performed using a speciﬁc antibody to phospho-c-Fos (Ser32) and qPCR using primers to mouse negative control binding site and the Il6 promoter. n ¼ 3, Student’s t test: ****p < 0.0001, **p < 0.01, *p < 0.05.

Article Snippet: Recombinant mouse WNT5B (rWNT5B; Cat. # 3006-WN) was acquired from R&D Systems.

Techniques: Activity Assay, Transfection, Luciferase, Plasmid Preparation, Western Blot, Derivative Assay, Negative Control, Binding Assay

Figure 7. WNT5B inhibits E2-induced ALPL expression via SIN3A (A and B) mOBs (A) or U2OS-ERa cells (B) were treated with EtOH or 10 nM E2 in the presence or absence of 50 ng/mL rWNT5B for 4 days. Then, alkaline phos- phatase (ALP) activity was detected and was normalized with total protein. (C) Expression of ALPL also was measured in U2OS-ERa cells. (D) Diagram represents ALPL enhancers in U2OS-ERa cells. U2OS-ERa cells were treated with PBS/EtOH (Ctrl), 10 nM E2, 50 ng/mL rWNT5B, or E2 with rWNT5B for 45 min. (E and F) ChIP was performed using an antibody to (E) ERa or (F) SIN3A. qPCR was performed with primers to the ALPL enhancers and normalized to the b-actin (ACTB) promoter. (G) Co-immunoprecipitations were per- formed with an antibody to SIN3A before blotting with an antibody to ERa or IgG in U2OS-ERa cells. (H) mOBs were treated with 50 ng/mL rWNT5B for 0 and 15 min, and then were incubated with or without calf in- testinal protease (CIP) in vitro before detect- ing phospho-CDK5 (Tyr15) and SIN3A by immunoblotting and normalized to b-actin (BA) by ImageJ. Three different bio- logical replicates were tested and a repre- sentative image from one replicate is pre- sented. n ¼ 3, Student’s t test: **p < 0.01, *p < 0.05.

Journal: American journal of human genetics

Article Title: Estrogen receptor alpha and NFATc1 bind to a bone mineral density-associated SNP to repress WNT5B in osteoblasts.

doi: 10.1016/j.ajhg.2021.11.018

Figure Lengend Snippet: Figure 7. WNT5B inhibits E2-induced ALPL expression via SIN3A (A and B) mOBs (A) or U2OS-ERa cells (B) were treated with EtOH or 10 nM E2 in the presence or absence of 50 ng/mL rWNT5B for 4 days. Then, alkaline phos- phatase (ALP) activity was detected and was normalized with total protein. (C) Expression of ALPL also was measured in U2OS-ERa cells. (D) Diagram represents ALPL enhancers in U2OS-ERa cells. U2OS-ERa cells were treated with PBS/EtOH (Ctrl), 10 nM E2, 50 ng/mL rWNT5B, or E2 with rWNT5B for 45 min. (E and F) ChIP was performed using an antibody to (E) ERa or (F) SIN3A. qPCR was performed with primers to the ALPL enhancers and normalized to the b-actin (ACTB) promoter. (G) Co-immunoprecipitations were per- formed with an antibody to SIN3A before blotting with an antibody to ERa or IgG in U2OS-ERa cells. (H) mOBs were treated with 50 ng/mL rWNT5B for 0 and 15 min, and then were incubated with or without calf in- testinal protease (CIP) in vitro before detect- ing phospho-CDK5 (Tyr15) and SIN3A by immunoblotting and normalized to b-actin (BA) by ImageJ. Three different bio- logical replicates were tested and a repre- sentative image from one replicate is pre- sented. n ¼ 3, Student’s t test: **p < 0.01, *p < 0.05.

Article Snippet: Recombinant mouse WNT5B (rWNT5B; Cat. # 3006-WN) was acquired from R&D Systems.

Techniques: Expressing, Activity Assay, Incubation, In Vitro, Western Blot

Figure 8. Model of the regulation of WNT5B expression at SNP rs2887571 and the signaling pathway of WNT5B in osteoblasts (A) The molecular mechanisms of ERa and NFATc1 at SNP rs2887571 in cells with homozygous AA (right) or homozygous GG (left) at rs2887571. (Top) Homozygous GG has increased ERa, NFATc1 and SIN3A compared to homozygous AA, which re- sults in lower endogenous WNT5B expression due to the repres- sive effects of SIN3A. (Bottom) The presence of E2 recruits SIN3A to suppress the expression of WNT5B in both genotypes, with increased suppression in cells with GG due to increased recruit- ment of SIN3A. (B) WNT5B binds with ROR1/2 then activates DVL2/3, RAC1/ CDC42, p-JNK, and p-c-Fos. Phosphorylation of SIN3A by CDK5 results in proteasome degradation. WNT5B inhibits phosphoryla- tion of CDK5 (Tyr15), resulting in accumulation of SIN3A. WNT5B also inhibits b-catenin activity in osteoblasts. Solid lines indicate the signaling pathways described in this study. The dashed line in- dicates the signaling that has been previously reported. P indicates phosphorylation. Created with BioRender.com

Journal: American journal of human genetics

Article Title: Estrogen receptor alpha and NFATc1 bind to a bone mineral density-associated SNP to repress WNT5B in osteoblasts.

doi: 10.1016/j.ajhg.2021.11.018

Figure Lengend Snippet: Figure 8. Model of the regulation of WNT5B expression at SNP rs2887571 and the signaling pathway of WNT5B in osteoblasts (A) The molecular mechanisms of ERa and NFATc1 at SNP rs2887571 in cells with homozygous AA (right) or homozygous GG (left) at rs2887571. (Top) Homozygous GG has increased ERa, NFATc1 and SIN3A compared to homozygous AA, which re- sults in lower endogenous WNT5B expression due to the repres- sive effects of SIN3A. (Bottom) The presence of E2 recruits SIN3A to suppress the expression of WNT5B in both genotypes, with increased suppression in cells with GG due to increased recruit- ment of SIN3A. (B) WNT5B binds with ROR1/2 then activates DVL2/3, RAC1/ CDC42, p-JNK, and p-c-Fos. Phosphorylation of SIN3A by CDK5 results in proteasome degradation. WNT5B inhibits phosphoryla- tion of CDK5 (Tyr15), resulting in accumulation of SIN3A. WNT5B also inhibits b-catenin activity in osteoblasts. Solid lines indicate the signaling pathways described in this study. The dashed line in- dicates the signaling that has been previously reported. P indicates phosphorylation. Created with BioRender.com

Article Snippet: Recombinant mouse WNT5B (rWNT5B; Cat. # 3006-WN) was acquired from R&D Systems.

Techniques: Expressing, Phospho-proteomics, Activity Assay, Protein-Protein interactions

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