Cell Signaling Technology

Product Pathways - Chromatin Regulation / Epigenetics

HMGA1 (D6A4) XP® Rabbit mAb #7777

No. Size Price
7777S 100 µl ( 10 western blots ) ¥3,750.00 现货查询 购买询价 防伪查询
7777T 20 µl ( 2 western blots ) ¥1,400.00 现货查询 购买询价 防伪查询
7777 carrier free & custom formulation / quantityemail request
Applications Dilution Species-Reactivity Sensitivity MW (kDa) Isotype
W 1:1000 Human,Monkey, Endogenous 18 Rabbit IgG
IP 1:200
IF-IC 1:3200

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

HMGA1 (D6A4) XP® Rabbit mAb recognizes endogenous levels of total HMGA1 protein, isoforms 1a and 1b. Based on sequence homology, this antibody is not predicted to cross-react with HMGA2.

HMGA1 (D6A4) XP® Rabbit mAb兔单抗能够识别内源性HMGA1总蛋白、异构体1a和1b。基于序列的同源性,预测该抗体不与HMGA2发生交叉反应。

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Gly68 of human HMGA1 protein.




Confocal immunofluorescent analysis of NCCIT (high expression; left) or MCF7 (low expression; right) cells, using HMGA1 (D6A4) XP® Rabbit mAb (green). Actin filaments were labeled with DY-554 phalloidin (red). Blue pseudocolor = DRAQ5® #4084 (fluorescent DNA dye).采用共聚焦免疫荧光术检测NCCIT(高表达;左)和MCF7细胞(低表达;右),使用的抗体为HMGA1 (D6A4) XP® Rabbit mAb (绿色)。肌动蛋白微丝使用DY-554 phalloidin进行标记(红色)。蓝色假彩色= DRAQ5® #40

Western Blotting

Western Blotting

Western blot analysis of extracts from various cell lines using HMGA1 (D6A4) XP® Rabbit mAb (upper) or β-Actin (D6A8) Rabbit mAb #8457 (lower).Western blot方法检测不同细胞系的提取物,使用的抗体为HMGA1 (D6A4) XP® Rabbit mAb (上图) or β-Actin (D6A8) Rabbit mAb #8457 (下图)。



Immunoprecipitation of HMGA1 from COS-7 cell extracts, using Rabbit (DA1E) mAb IgG XP® Isotype Control #3900 (lane 3) or HMGA1 (D6A4) XP® Rabbit mAb (lane 2). Lane 1 is 10% input. Western blot analysis was performed using HMGA1 (D6A4) XP® Rabbit mAb.从 COS-7细胞提取物中免疫沉淀HMGA1,使用的抗体为Rabbit (DA1E) mAb IgG XP® Isotype Control #3900 (lane3)或HMGA1 (D6A4) XP® Rabbit mAb (lane 2)。Lane 1为10% input。 使用HMGA1 (D6A4) XP® Rabbit mAb进行Western blot检测。


HMGA1, formerly known as HMG-I/Y, belongs to a family of high mobility group proteins that contain an AT-hook DNA binding domain. HMGA proteins are considered architectural transcription factors; they do not have direct transcriptional activation capacity, but instead regulate gene expression by changing DNA conformation through binding to AT-rich regions in the DNA and/or direct interaction with other transcription factors (1,2). HMGA1 is highly expressed during embryogenesis and in embryonic stem cells, but not in fully differentiated adult tissues (2-4). Research studies have shown that HMGA1 is over-expressed in rapidly dividing neoplastic cells and a wide variety of aggressive cancers, including thyroid, colon, breast, pancreas, and prostate (2-4). Investigators have shown that forced expression of HMGA1 induces cellular transformation and an epithelial-to-mesenchymal transition (EMT), while inhibition of HMGA1 expression blocks anchorage-independent cell growth and proliferation of cancer cells, suggesting that HMGA1 contributes to carcinogenesis by inducing and maintaining a de-differentiated, highly proliferative cell state (5-8).

HMGA1,原名为HMG-I/Y,属于含有一个AT-hook DNA结合结构域的高迁移率族蛋白家族。HMGA蛋白被认为是架构转录因子;他们不具备直接的转录激活能力,但是相反他们能够通过结合到DNA富含AT的区域来改变DNA构象或者直接与其他转录因子相互作用从而调控基因表达(1,2)。HMGA1在胚胎干细胞以及在胚胎形成期间会高度表达,但不是在完全分化的成年组织中(2-4)。研究发现,HMGA1在快速分裂的肿瘤细胞以及很多侵略性癌症包括甲状腺癌、结肠癌、乳腺癌、胰腺癌以及前列腺癌中一些中会过表达(2-4)。研究者还发现强制表达HMGA1会导致细胞转化和上皮-间充质转变(EMT),而抑制HMGA1表达会阻断非贴壁依赖性细胞的生长以及癌细胞的增殖,这意味着HMGA1通过降低和维持一种去分化的高度增殖的细胞状态来促进肿瘤发生(5-8)。

  1. Cleynen, I. and Van de Ven, W.J. (2008) Int J Oncol 32, 289-305.
  2. Resar, L.M. (2010) Cancer Res 70, 436-9.
  3. Chiappetta, G. et al. (1996) Oncogene 13, 2439-46.
  4. Ben-Porath, I. et al. (2008) Nat Genet 40, 499-507.
  5. Wood, L.J. et al. (2000) Mol Cell Biol 20, 5490-502.
  6. Wood, L.J. et al. (2000) Cancer Res 60, 4256-61.
  7. Xu, Y. et al. (2004) Cancer Res 64, 3371-5.
  8. Scala, S. et al. (2000) Proc Natl Acad Sci U S A 97, 4256-61.

Application References

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