Date published: 2026-5-9

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GATAD2A Activators

The chemical class of GATAD2A activators is not well-defined due to the indirect nature of their activation mechanisms. However, the chemicals listed above are connected by their ability to influence epigenetic modifications and transcription factor activity, which can, in turn, affect the functional activity of GATAD2A. These compounds operate through distinct cellular pathways: 5-Azacytidine disrupts DNA methylation patterns; histone deacetylase inhibitors like Trichostatin A and SAHA alter histone acetylation levels; Disulfiram can interact with metal-dependent molecules; Parthenolide interferes with NF-kB signaling; and Retinoic Acid modulates gene expression via retinoic acid receptors. These mechanisms of action converge on the potential modulation of GATAD2A activity by altering its expression levels or its ability to interact with chromatin and DNA.

These activators represent a heterogeneous group of compounds with varying biochemical properties and mechanisms. Their commonality lies in their potential to indirectly promote a transcriptional environment that is less conducive to the repressive functions of GATAD2A, either by changing the epigenetic landscape or by affecting other cellular signaling pathways that can indirectly influence the activity or expression of GATAD2A. The functional implications of these compounds are complex and context-dependent, but all can lead to changes in gene expression that might impinge on the activity of GATAD2A.

SEE ALSO...

Product NameCAS #Catalog #QUANTITYPriceCitationsRATING

5-Azacytidine

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

5-Azacytidine is a chemical analog of cytidine that can be incorporated into DNA and RNA. When incorporated into DNA, it inhibits DNA methyltransferases, leading to a reduction in DNA methylation. Hypomethylated states of gene promoter regions can alter the binding affinity of transcriptional repressors like GATAD2A, potentially increasing gene expression by reducing GATAD2A-mediated repression.

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 is a histone deacetylase inhibitor that alters chromatin structure by preventing the removal of acetyl groups from histones. This causes chromatin to adopt a more relaxed, open conformation, which can interfere with the ability of transcriptional repressors like GATAD2A to bind DNA effectively, potentially reducing their repressive impact on gene expression.

Suberoylanilide Hydroxamic Acid

149647-78-9sc-220139
sc-220139A
100 mg
500 mg
$133.00
$275.00
37
(2)

SAHA, or Vorinostat, is another histone deacetylase inhibitor with a mechanism of action similar to Trichostatin A. By inhibiting deacetylation, SAHA can disrupt the function of GATAD2A by promoting a transcriptionally active state of chromatin, possibly impairing GATAD2A's repressive functions.

Disulfiram

97-77-8sc-205654
sc-205654A
50 g
100 g
$53.00
$89.00
7
(1)

Disulfiram can chelate metal ions and form complexes that may interfere with the function of metal-dependent transcriptional repressors. While not directly linked to GATAD2A, such effects could theoretically perturb its activity by altering metal homeostasis in cells.

Parthenolide

20554-84-1sc-3523
sc-3523A
50 mg
250 mg
$81.00
$306.00
32
(2)

Parthenolide is a sesquiterpene lactone known to inhibit NF-kB signaling. While GATAD2A is not directly involved in this pathway, inhibition of NF-kB can have widespread effects on the expression of many genes, potentially including those that interact with or regulate GATAD2A.

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, a metabolite of vitamin A, binds to retinoic acid receptors (RARs) and can regulate gene expression. Though not a direct activator of GATAD2A, it can modulate chromatin structure and the activity of different transcription factors, which could in turn affect the function of GATAD2A by altering the transcriptional landscape in which it operates.