EVA1B inhibitors encompass a range of chemical compounds that modulate specific cellular signaling pathways leading to the decreased functional activity of EVA1B. For instance, Rapamycin and PP242, both mTOR inhibitors, suppress the mTOR signaling pathway, which is essential for cellular anabolic processes, thereby promoting autophagy-a cellular state where EVA1B's role is mitigated. This shift in cellular state leads to a diminished dependency on EVA1B's normal homeostatic functions. Similarly, compounds like LY 294002 and Wortmannin, which are PI3K inhibitors, hinder the PI3K/AKT pathway, a critical route for cell survival and proliferation, thus indirectly attenuating EVA1B's contribution to these processes. In contrast, by obstructing early stages of autophagy, 3-Methyladenine (3-MA), Spautin-1, and Bafilomycin A1 lead to a reduction in EVA1B's function as they interfere with autophagosome formation and lysosomal activity, core elements of EVA1B's functional landscape.
Further expanding the spectrum of EVA1B inhibition, Chloroquine disrupts the autophagic process by impairing autophagosome-lysosome fusion, thereby diminishing EVA1B's role within autophagy. MAPK pathway inhibitors like SB 203580, U0126, and PD 98059 diminish EVA1B's activity by dampening the cellular stress response and ERK signaling pathways, which are potentially connected to the functional modulation of EVA1B. Additionally, SBI-0206965, a selective ULK1 inhibitor, compromises the initiation phase of autophagy, further contributing to the reduction of EVA1B's functional activity. Each of these inhibitors acts on distinct but interconnected biochemical pathways, collectively contributing to a comprehensive inhibitory effect on EVA1B's role within cellular homeostasis and stress response mechanisms.
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Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
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Rapamycin | 53123-88-9 | sc-3504 sc-3504A sc-3504B | 1 mg 5 mg 25 mg | $62.00 $155.00 $320.00 | 233 | |
Rapamycin, an mTOR inhibitor, impedes the mTOR pathway which is crucial for cell growth and proliferation. As EVA1B is involved in cell autophagy, inhibition of mTOR by rapamycin would enhance autophagic processes, thereby reducing the functional activity of EVA1B as cells shift towards catabolism rather than the normal homeostatic functions where EVA1B operates. | ||||||
LY 294002 | 154447-36-6 | sc-201426 sc-201426A | 5 mg 25 mg | $121.00 $392.00 | 148 | |
LY 294002, a PI3K inhibitor, disrupts the PI3K/AKT pathway. Since EVA1B is implicated in cell survival processes, inhibiting PI3K would attenuate AKT signaling, thus diminishing EVA1B's role in promoting cell survival and potentially increasing autophagic activity which often accompanies reduced AKT pathway signaling. | ||||||
Wortmannin | 19545-26-7 | sc-3505 sc-3505A sc-3505B | 1 mg 5 mg 20 mg | $66.00 $219.00 $417.00 | 97 | |
Wortmannin, another PI3K inhibitor, similarly to LY294002, disrupts the PI3K/AKT signaling pathway. This inhibition could lead to an indirect decrease in EVA1B's survival-promoting activities by shifting cellular equilibrium towards autophagy, where the functional role of EVA1B is not central. | ||||||
Autophagy Inhibitor, 3-MA | 5142-23-4 | sc-205596 sc-205596A | 50 mg 500 mg | $56.00 $256.00 | 113 | |
3-Methyladenine (3-MA) is known to inhibit autophagy by blocking autophagosome formation. By inhibiting autophagy, 3-MA would reduce the cellular context in which EVA1B operates, consequently diminishing its functional activity related to autophagic processes. | ||||||
Spautin-1 | 1262888-28-7 | sc-507306 | 10 mg | $165.00 | ||
Spautin-1 promotes the degradation of PI3K class III and Vps34, leading to an inhibition of autophagy. This action reduces the dependency of the cell on autophagic mechanisms where EVA1B is involved, thus diminishing EVA1B's functional activity. | ||||||
Chloroquine | 54-05-7 | sc-507304 | 250 mg | $68.00 | 2 | |
Chloroquine, a known autophagy inhibitor, functions by increasing the pH in lysosomes, which impairs autophagosome fusion and degradation. As EVA1B is associated with autophagic pathways, chloroquine's effect would lead to a functional inhibition of EVA1B by disrupting the autophagic process it is involved in. | ||||||
SB 203580 | 152121-47-6 | sc-3533 sc-3533A | 1 mg 5 mg | $88.00 $342.00 | 284 | |
SB 203580, a p38 MAPK inhibitor, would interfere with stress response signaling pathways. By inhibiting p38 MAPK, the cellular response to stress, which may include autophagic pathways involving EVA1B, would be dampened, thereby diminishing EVA1B's role in these processes. | ||||||
PD 98059 | 167869-21-8 | sc-3532 sc-3532A | 1 mg 5 mg | $39.00 $90.00 | 212 | |
PD 98059 is a MEK inhibitor that specifically blocks MEK activation, leading to a reduction in ERK phosphorylation and activity. This would likely lead to altered cellular signaling where EVA1B is involved, indirectly diminishing its functional activity. | ||||||
Bafilomycin A1 | 88899-55-2 | sc-201550 sc-201550A sc-201550B sc-201550C | 100 µg 1 mg 5 mg 10 mg | $96.00 $250.00 $750.00 $1428.00 | 280 | |
Bafilomycin A1 is a V-ATPase inhibitor that prevents the acidification of organelles and inhibits autophagy by preventing autophagosome-lysosome fusion. This would inhibit the functional activity of EVA1B by disrupting the autophagic processes it is involved in. | ||||||
PP242 | 1092351-67-1 | sc-301606A sc-301606 | 1 mg 5 mg | $56.00 $169.00 | 8 | |
PP242 is an ATP-competitive mTOR inhibitor that robustly inhibits both mTORC1 and mTORC2 complexes. Its action leads to a downregulation of cellular growth signaling pathways, indirectly reducing the functional activity of EVA1B by promoting catabolic processes over anabolic processes such as those in which EVA1B participates. |