Date published: 2026-4-25

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HoxD11 Activators

HoxD11 is a member of the Hox gene family, which plays a crucial role in the development of body plans and the segmentation of embryonic structures across a wide range of species. As a transcription factor, HoxD11 is specifically important in the morphogenesis of the vertebrate limb and the axial skeleton. It is one of the key genes involved in patterning the anterior-posterior axis and in limb development, where it helps to define the correct number and position of future bone elements. The precise spatial and temporal expression of HoxD11 is essential for the proper development of these structures, and deviations in its expression can lead to significant morphological changes. The expression of HoxD11 is tightly controlled by a variety of regulatory mechanisms, including upstream signaling pathways, the presence of enhancers and silencers within its gene regulatory network, and epigenetic modifications that can either promote or silence its transcription.

In the realm of molecular biology, there are specific chemical compounds that are known to act as activators, potentially inducing the expression of genes such as HoxD11. Retinoic acid, for example, is a derivative of vitamin A that can bind to retinoic acid receptors and trigger the transcription of certain Hox genes, including HoxD11, especially during early embryonic development. Other activators, like the DNA methyltransferase inhibitor 5-Azacytidine, can induce expression by causing demethylation of DNA in the gene promoter regions, which may lead to the activation of HoxD11 transcription. Histone deacetylase inhibitors, such as Trichostatin A, promote a more open and accessible chromatin structure, which can enhance the transcription of genes like HoxD11. Additionally, hormonal signals such as estradiol and dihydrotestosterone (DHT) can also play a role in the cell-type specific regulation of HoxD11 expression, by binding to their respective receptors and influencing gene activation. Essential nutrients like folate are implicated in one-carbon metabolism, which contributes to the methylation of DNA and can have downstream effects on gene expression, including that of HoxD11. Lastly, Lithium Chloride, known for its influence on the Wnt signaling pathway, may also play a role in the intricate regulation of HoxD11, though its mechanism is complex and involves a cascade of intracellular events. Each of these activators operates through a distinct molecular mechanism, revealing the multifaceted nature of gene expression regulation.

Product NameCAS #Catalog #QUANTITYPriceCitationsRATING

Retinoic Acid, all trans

302-79-4sc-200898
sc-200898A
sc-200898B
sc-200898C
500 mg
5 g
10 g
100 g
$66.00
$325.00
$587.00
$1018.00
28
(1)

Retinoic acid interacts with specific retinoic acid receptors within the cell, which can upregulate the transcription of HoxD11, particularly during the differentiation of limbs.

5-Azacytidine

320-67-2sc-221003
500 mg
$280.00
4
(1)

By inhibiting DNA methyltransferases, 5-Azacytidine can cause the demethylation of gene promoter regions, potentially stimulating the transcription of HoxD11.

Trichostatin A

58880-19-6sc-3511
sc-3511A
sc-3511B
sc-3511C
sc-3511D
1 mg
5 mg
10 mg
25 mg
50 mg
$152.00
$479.00
$632.00
$1223.00
$2132.00
33
(3)

Trichostatin A prevents the deacetylation of histone proteins, thus enhancing histone acetylation levels and enabling the transcription machinery to access the HoxD11 gene more easily, increasing its expression.

β-Estradiol

50-28-2sc-204431
sc-204431A
500 mg
5 g
$63.00
$182.00
8
(1)

β-Estradiol binds to estrogen receptors which can lead to the selective upregulation of genes, including HoxD11, during processes such as sexual differentiation.

Folic Acid

59-30-3sc-204758
10 g
$73.00
2
(1)

Folate participates in the one-carbon metabolism that is essential for DNA methylation, which can stimulate the expression of HoxD11 by altering epigenetic marks.

Lithium

7439-93-2sc-252954
50 g
$214.00
(0)

Lithium Chloride can activate the Wnt signaling pathway, which has been shown to upregulate the expression of several Hox genes, possibly including HoxD11.