Cell Signaling Technology

Product Pathways - Chromatin Regulation / Epigenetics

JMJD1B/JHDM2B Antibody #2621

No. Size Price
2621S 100 µl ( 10 western blots ) ¥3,100.00 现货查询 购买询价
2621 carrier free & custom formulation / quantityemail request
Applications Dilution Species-Reactivity Sensitivity MW (kDa) Isotype
W 1:1000 Human,Mouse,Rat,Monkey, Endogenous 220 Rabbit
IP 1:25
IF-IC 1:100

Species cross-reactivity is determined by western blot.

Applications Key: W=Western Blotting, IP=Immunoprecipitation, IF-IC=Immunofluorescence (Immunocytochemistry),


Species predicted to react based on 100% sequence homology: Bovine,

Specificity / Sensitivity

JMJD1B/JHDM2B Antibody detects endogenous levels of JMJD1B protein (all three isoforms).

JMJD1B/JHDM2B Antibody能够检测内源性JMJD1B蛋白水平(所有三个亚型)。

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to the human JMJD1B protein. Antibodies are purified by peptide affinity chromatography.




Confocal immunofluorescent analysis of HeLa cells using JMJD1B/JHDM2B Antibody (green). Actin filaments have been labeled with Alexa Fluor® 555 phalloidin (red).

使用JMJD1B/JHDM2B Antibody (绿色)标记,共聚焦免疫荧光分析HeLa细胞。Alexa Fluor® 555 phalloidin标记微丝蛋白(红色)。

Western Blotting

Western Blotting

Western blot analysis of whole cell lysates from HeLa, RAW and COS cells using JMJD1B/JHDM2B Antibody.

使用JMJD1B/JHDM2B Antibody,免疫印迹(Western blot)分析HeLa、RAW和COS细胞中JMJD1B/JHDM2B的蛋白水平。


The methylation state of lysine residues in histone proteins is a major determinant of the formation of active and inactive regions of the genome and is crucial for the proper programming of the genome during development (1,2). Jumonji C (JmjC) domain-containing proteins represent the largest class of potential histone demethylase proteins (3). The JmjC domain of several proteins has been shown to catalyze the demethylation of mono-, di-, and tri-methyl lysine residues via an oxidative reaction that requires iron and α-ketoglutarate (3). Based on homology, both humans and mice contain at least 30 such proteins, which can be divided into seven separate families (3). The JMJD1 (Jumonji domain-containing protein 1) family, also known as JHDM2 (JmjC domain-containing histone demethylation protein 2) family, contains four members: hairless (HR), JMJD1A/JHDM2A, JMJD1B/JHDM2B, and JMJD1C/JHDM2C. Hairless is expressed in the skin and brain and acts as a co-repressor of the thyroid hormone receptor (4-6). Mutations in the hairless gene cause alopecia in both mice and humans (4,5). JMJD1A is expressed in meiotic and post-meiotic male germ cells, contributes to androgen receptor-mediated gene regulation, and is required for spermatogenesis (7-9). It has also been identified as a downstream target of OCT4 and STAT3 and is critical for the regulation of self-renewal in embryonic stem cells (10,11). JMJD1B is a more widely expressed family member and is frequently deleted in myeloid leukemia (12). JMJD1C (also known as TRIP8) is a co-factor of both the androgen and thyroid receptors and has a potential link to autism (13-15). Members of the JMJD1/JHDM2 family have been shown to demethylate mono-methyl and di-methyl histone H3 (Lys9) (3,8).

组蛋白赖氨酸的甲基化水平对于基因组的活化和非活化区域的形成是主要决定因素,并且在发育期间对于基因组的正确进程起着关键作用(1,2)。包含蛋白质的Jumonji C (JmjC)区域代表最大的潜在组蛋白去乙酰化酶蛋白(3)。JmjC区域通过氧化反应能催化单、双和三甲基化的赖氨酸残基的去乙甲基化,这种氧化反应需要铁离子和α-酮戊二酸(3)。基于同源性,人源和小鼠都包含至少30种这样蛋白质,这能够被分为7个不同的家族(3)。JMJD1 (Jumonji domain-containing protein 1) 家族又称为JHDM2 (JmjC domain-containing histone demethylation protein 2)家族,其包含四个成员:hairless (HR)、JMJD1A/JHDM2A、JMJD1B/JHDM2B和JMJD1C/JHDM2C。Hairless蛋白在皮肤和大脑组织中表达,并且作为甲状腺激素受体的共抑制剂(4-6)。在小鼠和人源中hairless基因突变引起脱发(4,5)。JMJD1A在减数分裂和减数分裂的男性生殖细胞中表达,这有助于雄激素受体介导基因调节,并且对于精子形成是需要的(7-9)。它也被鉴定作为OCT4和STAT3的下游靶基因,并且在胚胎干细胞中自我更新的调节里起到关键作用(10,11)。JMJD1B蛋白是一个广泛表达的家族成员,并且在骨髓性白血病中频繁缺失(12)。JMJD1C (又称为TRIP8)是一个雄激素和甲状腺受体的共同因子,并且它潜在的联系到自闭症(13-15)。JMJD1/JHDM2家族成员已经证明可以使单甲基化和双甲基化的histone H3 (Lys9)去甲基化(3,8)。

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  2. Lin, W. and Dent, S.Y. (2006) Curr Opin Genet Dev 16, 137-42.
  3. Klose, R.J. et al. (2006) Nat Rev Genet 7, 715-27.
  4. Cachon-Gonzalez, M.B. et al. (1994) Proc Natl Acad Sci USA 91, 7717-21.
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  9. Okada, Y. et al. (2007) Nature 450, 119-23.
  10. Loh, Y.H. et al. (2007) Genes Dev 21, 2545-57.
  11. Ko, S.Y. et al. (2006) Cell Struct Funct 31, 53-62.
  12. Hu, Z. et al. (2001) Oncogene 20, 6946-54.
  13. Lee, J.W. et al. (1995) Mol Endocrinol 9, 243-54.
  14. Wolf, S.S. et al. (2007) Arch Biochem Biophys 460, 56-66.
  15. Castermans, D. et al. (2007) Eur J Hum Genet 15, 422-31.

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