Date published: 2026-5-9

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HiNF-P Activators

Chemical activators of HiNF-P play a role in modulating the gene expression patterns essential for cell cycle progression and regulation. Retinoic acid, by influencing gene activation involved in cell cycle regulation, can enhance the activity of HiNF-P, especially by promoting entry into the S phase, where HiNF-P is most active. Similarly, 5-Azacytidine acts through inhibition of DNA methyltransferase, leading to hypomethylation of genes and potentially increasing the expression and functional activity of HiNF-P. Forskolin, through the activation of adenylate cyclase, raises cAMP levels, thereby activating the protein kinase A (PKA) signaling pathway, which can phosphorylate transcription factors and proteins involved in cell cycle progression, potentially enhancing HiNF-P function. Epidermal Growth Factor (EGF) engages its receptor and initiates a signaling cascade conducive to cell proliferation, indirectly necessitating the activity of HiNF-P due to the increased demand for cell cycle progression proteins.

Trichostatin A (TSA) and sodium butyrate, both histone deacetylase inhibitors, lead to a more relaxed chromatin state, which can result in increased transcription of various genes, including HINFP, and subsequent functional activation of HiNF-P. Phorbol 12-myristate 13-acetate (PMA) activates protein kinase C (PKC), involved in cell cycle regulation, which can also lead to the functional activation of HiNF-P. Lithium chloride, through the inhibition of glycogen synthase kinase-3 (GSK-3), can result in the stabilization and accumulation of β-catenin, which may augment HiNF-P expression by promoting gene expression linked to the cell cycle. Dibutyryl-cAMP, a membrane-permeable cAMP analog, can activate PKA and lead to the functional activation of HiNF-P by promoting the phosphorylation of cell cycle-related transcription factors. Thymidine, by synchronizing cells at the S phase, can amplify the demand for HiNF-P's activity, which is crucial for histone gene transcription during DNA replication. Lastly, β-estradiol, through estrogen receptor signaling, modulates gene transcription and can lead to the functional activation of HiNF-P by upregulating transcription factors involved in cell cycle progression. Dimethyl sulfoxide (DMSO) influences differentiation pathways and gene expression, which may involve the activation of HiNF-P as cells undergo changes that require histone gene transcription.

SEE ALSO...

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 can activate genes involved in cell cycle regulation. As HiNF-P is a cell cycle regulator that promotes the expression of histone H4 genes during the S phase, retinoic acid may enhance HiNF-P’s activity by upregulating pathways that lead to S phase entry, where HiNF-P is most active.

5-Azacytidine

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

5-Azacytidine, a DNA methyltransferase inhibitor, can lead to the hypomethylation of genes, potentially including HINFP, resulting in its increased expression and subsequent functional activation. This compound affects the epigenetic state of the cell, thereby possibly upregulating HiNF-P expression as part of a broader change in gene expression.

Forskolin

66575-29-9sc-3562
sc-3562A
sc-3562B
sc-3562C
sc-3562D
5 mg
50 mg
1 g
2 g
5 g
$78.00
$153.00
$740.00
$1413.00
$2091.00
73
(3)

Forskolin activates adenylate cyclase, increasing cAMP levels, which can enhance the protein kinase A (PKA) signaling pathway. PKA can phosphorylate various transcription factors and proteins that are involved in cell cycle progression, potentially leading to the functional activation of HiNF-P by promoting cell cycle events where HiNF-P is required.

PMA

16561-29-8sc-3576
sc-3576A
sc-3576B
sc-3576C
sc-3576D
1 mg
5 mg
10 mg
25 mg
100 mg
$41.00
$132.00
$214.00
$500.00
$948.00
119
(6)

PMA activates protein kinase C (PKC), which is involved in various signaling pathways, including those that regulate the cell cycle. As HiNF-P is involved in cell cycle regulation, the activation of PKC by PMA can lead to the functional activation of HiNF-P indirectly by promoting cell cycle progression.

Lithium

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

Lithium chloride can inhibit glycogen synthase kinase-3 (GSK-3), which is involved in Wnt signaling. Inhibition of GSK-3 can result in the stabilization and accumulation of β-catenin, a coactivator for transcription factors that may indirectly increase HiNF-P expression and activation by promoting gene expression associated with the cell cycle.

Dibutyryl-cAMP

16980-89-5sc-201567
sc-201567A
sc-201567B
sc-201567C
20 mg
100 mg
500 mg
10 g
$47.00
$136.00
$492.00
$4552.00
74
(7)

Dibutyryl-cAMP is a cAMP analog that can permeate cell membranes and activate PKA. It can indirectly lead to the functional activation of HiNF-P by promoting phosphorylation and activation of transcription factors involved in the cell cycle, where HiNF-P function is critical.

Thymidine

50-89-5sc-296542
sc-296542A
sc-296542C
sc-296542D
sc-296542E
sc-296542B
1 g
5 g
100 g
250 g
1 kg
25 g
$49.00
$73.00
$270.00
$458.00
$1758.00
$114.00
16
(1)

Thymidine is a nucleoside that, when added to cells, can synchronize them at the S phase of the cell cycle. Synchronizing cells at the S phase can lead to increased demand and functional activation of HiNF-P, which is essential for histone gene transcription during DNA replication.

β-Estradiol

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

β-estradiol can modulate the transcription of various genes through estrogen receptor signaling. It may lead to the functional activation of HiNF-P by upregulating transcription factors and coactivators involved in cell cycle progression that interact with or regulate HiNF-P activity.

Dimethyl Sulfoxide (DMSO)

67-68-5sc-202581
sc-202581A
sc-202581B
100 ml
500 ml
4 L
$31.00
$117.00
$918.00
136
(6)

DMSO can influence gene expression and differentiation pathways. It may lead to the functional activation of HiNF-P through the induction of cellular pathways that require the transcriptional activation of cell cycle-regulated genes, of which HiNF-P is a