- PA1-41056 - Invitrogen Antibodies HDAC6 antibody

Submitted references HDAC6 inactivates Runx2 promoter to block osteogenesis of bone marrow stromal cells in age-related bone loss of mice.

Ma C, Gao J, Liang J, Dai W, Wang Z, Xia M, Chen T, Huang S, Na J, Xu L, Feng S, Dai K, Liu G
Stem cell research & therapy 2021 Aug 28;12(1):484

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Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Western blot analysis of HDAC-6 in NIH 3T3 cell lysate probed with a HDAC6 polyclonal antibody (Product # PA1-41056).

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Western blot analysis of HDAC6 in NIH-3T3 cell lysate. Sample was incubated in HDAC6 polyclonal antibody (Product # PA1-41056).

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Western blot analysis of HDAC6 in 0.5 mg/mL NIH-3T3 lysate. Samples were incubated in HDAC6 polyclonal (Product # PA1-41056). This experiment was performed under reducing conditions using the 12-230 kDa separation system.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Fig. 4 Competitive binding of HDAC6 and AR on Runx2 promoter to modulate Runx2 expression in BMSCs. Runx2 promoter (- 1280 bp ~ + 270 bp) deletion mutant-driven luciferase vectors were established ( A ). Luciferase activity of every vector was measured by transient reporter assay in BMSCs from young mice ( B ). Runx2 promoter (- 347 bp ~ - 1 bp) deletion mutant-driven luciferase vectors were established ( C ). Luciferase activity of every vector was measured in BMSCs young mice ( D ). Luciferase activity of Runx2 promoter (- 327 bp ~ - 1 bp)-driven reporter vector was measured in response to AR-WT or AR-DN co-transfection ( E ). ChIP was employed to evaluate AR and HDAC6 occupancy of the Runx2 proximal promoter in BMSCs from young and aged mice with and without osteogenic induction ( F ). ChIP was employed to evaluate AR and HDAC6 occupancy of the Runx2 proximal promoter in response to AR-WT or AR-DN overexpression ( G ). Lentivirus vector loading siRNA against HDAC6 was employed to knockdown HDAC6 expression ( H ). ChIP was employed to evaluate AR and HDAC6 occupancy of the Runx2 proximal promoter in response to HDAC6 knockdown ( I ). Luc: luciferase, AR: androgen receptor, AR-WT: wild type AR, AR-DN: dominant negative AR, PC: positive control, NC: negative control. In transient reporter assay, the results were expressed as fold changes in relative luciferase unit (RLU) of every vector relative to empty luciferase vector. Data are shown as the mean +- SD. * p < 0.05, ** p

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Fig. 5 Runx2 expression activation in response to HDAC6 inhibition in BMSCs from aged mice. Lentivirus vector loading siRNA against HDAC6 was employed to knockdown HDAC6 expression in BMSCs from aged mice. Then ChIP assays were used to examine HDAC6 ( A ), acetylated H3K9/K14 ( B ) , acetylated H4K12 ( C ), and phosphorylated RNA polymerase II ( D ) occupancy in the Runx2 promoter regions. Quantitative RT-PCR was employed to measure Runx2 expression in BMSCs from aged mice in response to HDAC6 knockdown with and without osteogenic induction ( E ). ChIP assays were used to examine HDAC6 ( F ), acetylated H3K9/K14 ( G ) , acetylated H4K12 ( H ), and phosphorylated RNA polymerase II ( I ) occupancy in the Runx2 promoter regions in response to tubastatin A treatment. Quantitative RT-PCR was employed to measure Runx2 expression in BMSCs from aged mice in response to tubastatin A treatment with and without osteogenic induction ( J ). Data are shown as the mean +- SD. * p < 0.05, ** p < 0.01, *** p < 0.001

PA1-41056

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