Chemical inhibitors of APM2 function by interfering with various cellular signaling pathways that are essential for adipocyte differentiation, glucose homeostasis, and lipid metabolism. Wortmannin and LY294002 are notable for their ability to inhibit the phosphoinositide 3-kinases (PI3K), which play a critical role in the PI3K/AKT pathway, a pivotal signaling axis in the regulation of glucose uptake and adipocyte differentiation where APM2 is active. By impeding this pathway, these inhibitors can reduce the cellular uptake of glucose and subsequently the functional activity of APM2. Rapamycin, targeting the mammalian target of rapamycin (mTOR) pathway, operates in a different manner. It attenuates lipid synthesis and adipogenesis, processes in which APM2 is involved. As mTOR is central to protein synthesis and cell growth, its inhibition by Rapamycin leads to a direct reduction in APM2 activity in the context of lipid accumulation and adipocyte formation.
Furthermore, PD98059 and SB203580 obstruct the mitogen-activated protein kinase (MAPK) pathways but through different kinase targets. PD98059 selectively inhibits the MAP kinase kinase (MEK), which in turn inhibits the ERK/MAPK pathway, while SB203580 targets the p38 MAP kinase. Given that both ERK/MAPK and p38 MAP kinase are implicated in adipocyte differentiation, these inhibitors can decrease the role of APM2 in this process. GW9662 and T0070907, on the other hand, are antagonists of PPARγ, a nuclear receptor that regulates gene expression involved in adipogenesis. By blocking PPARγ, these compounds can suppress the upregulation of APM2 that typically occurs during the differentiation of adipocytes. Bisphenol A and Genistein disrupt hormonal signaling, with Bisphenol A interfering with estrogen receptor pathways and Genistein inhibiting tyrosine kinases, thereby limiting the functional role of APM2 in adipogenesis and lipid metabolism. Rosiglitazone, although a PPARγ agonist, can lead to feedback inhibition of adipocyte differentiation, thus affecting APM2 activity. Lastly, Niclosamide and Retinoic acid impact APM2 through energy modulation and receptor-mediated pathways, respectively. Niclosamide disrupts ATP production, critical for energy-dependent adipogenic processes where APM2 is implicated, whereas Retinoic acid modulates the retinoic acid receptors influencing adipocyte differentiation and consequently the role of APM2.
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Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
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Wortmannin | 19545-26-7 | sc-3505 sc-3505A sc-3505B | 1 mg 5 mg 20 mg | $66.00 $219.00 $417.00 | 97 | |
As an inhibitor of phosphoinositide 3-kinases (PI3K), Wortmannin inhibits the PI3K/AKT pathway which is crucial for various cellular processes including glucose uptake. Inhibition of this pathway can lead to reduced cellular glucose uptake, thereby inhibiting APM2, which plays a role in regulating adipocyte differentiation and glucose homeostasis. | ||||||
LY 294002 | 154447-36-6 | sc-201426 sc-201426A | 5 mg 25 mg | $121.00 $392.00 | 148 | |
LY294002 is another PI3K inhibitor that hinders the PI3K/AKT signaling pathway. By inhibiting this pathway, LY294002 can reduce the actions of APM2 related to glucose and lipid metabolism in adipocytes, as APM2 is implicated in these metabolic processes. | ||||||
Rapamycin | 53123-88-9 | sc-3504 sc-3504A sc-3504B | 1 mg 5 mg 25 mg | $62.00 $155.00 $320.00 | 233 | |
Rapamycin inhibits the mammalian target of rapamycin (mTOR) pathway, which is involved in lipid synthesis and adipogenesis. By inhibiting mTOR, Rapamycin can functionally inhibit APM2 by reducing lipid accumulation and adipocyte differentiation where APM2 is active. | ||||||
PD 98059 | 167869-21-8 | sc-3532 sc-3532A | 1 mg 5 mg | $39.00 $90.00 | 212 | |
PD98059 is a selective inhibitor of mitogen-activated protein kinase kinase (MEK), which subsequently inhibits the ERK/MAPK pathway. Since the ERK/MAPK pathway is involved in adipocyte differentiation, PD98059 can lead to functional inhibition of APM2 in the context of adipogenesis. | ||||||
SB 203580 | 152121-47-6 | sc-3533 sc-3533A | 1 mg 5 mg | $88.00 $342.00 | 284 | |
This compound inhibits p38 MAP kinase, which is involved in stress responses and adipocyte differentiation. By inhibiting p38 MAP kinase, SB203580 can result in the functional inhibition of APM2 by reducing adipogenic differentiation where APM2 is implicated. | ||||||
GW 9662 | 22978-25-2 | sc-202641 | 5 mg | $68.00 | 30 | |
GW9662 is a selective PPARγ antagonist. Since PPARγ is a master regulator of adipocyte differentiation and APM2 expression is upregulated during this process, GW9662 can functionally inhibit APM2 by blocking the adipogenic program. | ||||||
Bisphenol A | 80-05-7 | sc-391751 sc-391751A | 100 mg 10 g | $300.00 $490.00 | 5 | |
Bisphenol A can interfere with estrogen receptor signaling, which has been implicated in adipocyte differentiation. By disrupting estrogen receptor signaling, Bisphenol A can inhibit the functional role of APM2 in adipogenesis. | ||||||
Genistein | 446-72-0 | sc-3515 sc-3515A sc-3515B sc-3515C sc-3515D sc-3515E sc-3515F | 100 mg 500 mg 1 g 5 g 10 g 25 g 100 g | $26.00 $92.00 $120.00 $310.00 $500.00 $908.00 $1821.00 | 46 | |
Genistein is a tyrosine kinase inhibitor and also modulates estrogen receptor activity. By inhibiting tyrosine kinases involved in adipocyte differentiation, Genistein can inhibit the functional role of APM2 in adipogenesis and lipid metabolism. | ||||||
Rosiglitazone | 122320-73-4 | sc-202795 sc-202795A sc-202795C sc-202795D sc-202795B | 25 mg 100 mg 500 mg 1 g 5 g | $118.00 $320.00 $622.00 $928.00 $1234.00 | 38 | |
As a PPARγ agonist, Rosiglitazone normally stimulates adipogenesis, however, it can lead to negative feedback mechanisms that inhibit pathways of adipocyte differentiation. This complex interaction can result in functional inhibition of APM2 by limiting its role in adipocyte maturation and lipid storage. | ||||||
T0070907 | 313516-66-4 | sc-203287 | 5 mg | $138.00 | 1 | |
This is a potent and selective PPARγ antagonist. By inhibiting PPARγ, T0070907 can functionally inhibit APM2 by preventing adipocyte differentiation, a process in which APM2 is typically upregulated. |