产品: 磷酸化 HDAC5 (Ser498) 抗体
货号: AF3491
描述: Rabbit polyclonal antibody to Phospho-HDAC5 (Ser498)
应用: WB IHC IF/ICC
文献验证: WB
反应: Human, Mouse, Rat
预测: Zebrafish, Bovine, Horse, Sheep, Rabbit, Dog, Xenopus
蛋白号: Q9UQL6
RRID: AB_2834929

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 50ul RMB¥ 1300 现货
 100ul RMB¥ 2400 现货
 200ul RMB¥ 3200 现货

货期: 当天发货

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产品描述

来源:
Rabbit
应用:
WB 1:500-1:2000, IHC 1:50-1:200, IF/ICC 1:100-1:500
*The optimal dilutions should be determined by the end user.
*Tips:

WB: 适用于变性蛋白样本的免疫印迹检测. IHC: 适用于组织样本的石蜡(IHC-p)或冰冻(IHC-f)切片样本的免疫组化/荧光检测. IF/ICC: 适用于细胞样本的荧光检测. ELISA(peptide): 适用于抗原肽的ELISA检测.

反应:
Human, Mouse, Rat
克隆:
Polyclonal
特异性:
Phospho-HDAC5 (Ser498) Antibody detects endogenous levels of HDAC5 only when phosphorylated at Serine 498.
RRID:
AB_2834929
引用格式: Affinity Biosciences Cat# AF3491, RRID:AB_2834929.
偶联:
Unconjugated.
纯化:
The antibody is from purified rabbit serum by affinity purification via sequential chromatography on phospho-peptide and non-phospho-peptide affinity columns.
保存:
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
别名:

展开/折叠

Antigen NY CO 9; Antigen NY-CO-9; HD5; HDAC 5; HDAC5; HDAC5_HUMAN; Histone deacetylase 5; NY CO 9;

抗原和靶标

免疫原:

A synthesized peptide derived from human HDAC5 around the phosphorylation site of Ser498.

基因/基因ID:
描述:
HDAC9 a transcriptional regulator of the histone deacetylase family, subfamily 2. Deacetylates lysine residues on the N-terminal part of the core histones H2A, H2B, H3 AND H4.

研究领域

· Environmental Information Processing > Signal transduction > Apelin signaling pathway.   (View pathway)

· Human Diseases > Substance dependence > Alcoholism.

· Human Diseases > Infectious diseases: Viral > Human papillomavirus infection.

· Human Diseases > Infectious diseases: Viral > Epstein-Barr virus infection.

· Human Diseases > Cancers: Overview > Viral carcinogenesis.

文献引用

1). Wilson disease: intersecting DNA methylation and histone acetylation regulation of gene expression in a mouse model of hepatic copper accumulation. Cellular and Molecular Gastroenterology and Hepatology, 2021 (PubMed: 34098115) [IF=7.1]

Application: WB    Species: Mice    Sample: tx-j

Figure 2. Expression of HDAC4 and HDAC5 in mouse and HepG2 models of WD. Immunoblot densitometry analyses are normalized to β-ACTIN; data are represented as means ± SEM and statistical significance was determined by Student's t-test (*p< 0.05, **p< 0.01, and ****p< 0.0001). A: Total protein liver lysate densitometries for HDAC4 and HDAC5 protein expression in tx-j mice compared to C3H control at post-partum day 6 (PPD6; C3H n=4M/4F, tx-j n=5M/4F), 9 weeks (C3H n=4M/3F, tx-j n=4M/4F), 12 weeks (C3H n=4M/4F, tx-j n=4M/3F), and 24 weeks (C3H n=10M/12F, tx-j n=11M/11F). B: Total protein liver lysate densitometry analyses for HDAC4 and HDAC5 protein expression in 16-week old Atp7b -/- mice (n=7M/4F) and wild-type (WT, n=6M/5F). C: Immunohistochemical analysis of 24-week old C3H and tx-j mouse livers for HDAC5 (red) and DAPI (blue). Images display cytosolic and nuclear HDAC5 localization. White arrows indicate nuclei; scale bar = 50 µm. Bar graphs represent HDAC5 optical density in cytosol, nuclei, and the nucleus/cytosol ratio; n=3 mice/group, 60 cells/mouse. D: HDAC5 immunoblot of HepG2 cell lysates treated with CuSO 4 (0 to 100 µM; n=3 per treatment) for 24 hours. In this figure and all subsequent figures: C3H=C3HeB/FeJ control mice with normal copper metabolism, tx-j=C3He- Atp7b tx-j /J Jackson Laboratory toxic milk mouse model of Wilson disease (WD).

2). Antidepressant effect and mechanism of TMP269 on stress-induced depressive-like behavior in mice. Biochemical pharmacology, 2024 (PubMed: 38801927) [IF=5.3]

3). Interaction between A-kinase anchoring protein 5 and protein kinase A mediates CaMKII/HDAC signaling to inhibit cardiomyocyte hypertrophy after hypoxic reoxygenation. Cellular signalling, 2023 (PubMed: 36565899) [IF=4.4]

Application: WB    Species: Rat    Sample:

Fig. 2. AKAP5-mediated cardiomyocyte hypertrophy CaMKII/HDAC pathway. (A) Expression of CaMKII/HDAC and hypertrophy-related proteins after H/R and AKAP5 transfection; (B) Expression of CaMKII/HDAC proteins after H/R and siAKAP5 transfection and KN93(10 uM, 1 h) intervention. Analysis by one-way ANOVA, All data are presented as the means ± SD (n = 3). ***P < 0.001 and ****P < 0.0001 vs. the CON group; *P < 0.05, **P < 0.01 and ***P < 0.001 vs. the H/R group; **P < 0.01, ***P < 0.001 and ****P < 0.0001 vs. the H/R + siAKAP5 group. CON, normal control group; H/R, hypoxia-reoxygenation group; NC, empty vector group; siAKAP5, siRNA-AKAP5 transfection group; KN93, an inhibitor of calmodulin-dependent kinase type II; AKAP5, A-kinase anchoring protein 5; CaMKII, Ca2+/CaM-dependent protein kinase II; HDAC4 /5, Histone deacetylases 4/5; MEF2C, Myocyte enhancer factor 2C.

4). WNT10A induces apoptosis of senescent synovial resident stem cells through Wnt/calcium pathway-mediated HDAC5 phosphorylation in OA joints. BONE, 2021 (PubMed: 34000432) [IF=3.5]

Application: WB    Species: human    Sample: Sn-SMSCs

Fig. 4. |Histone deacetylase 5 (HDAC5) is involved in WNT10A-induced apoptosis of Sn-SMSCs: C: HDAC5 mRNA (left), protein (middle) levels. and HDAC5 phosphorylation at s498 (right); *P<0.05

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