ARHGEF17 Activators
ARHGEF17 can engage in various interactions to modulate its guanine nucleotide exchange factor (GEF) activity on Rho GTPases. GTPγS, a non-hydrolyzable GTP analog, can bind to G proteins and maintain them in an active state, thus enhancing the GEF activity of ARHGEF17. Similarly, Phorbol 12-myristate 13-acetate (PMA) activates protein kinase C (PKC), which can subsequently phosphorylate a range of downstream proteins, including those involved in the regulation of Rho GTPases. Such activation can lead to an upregulation of ARHGEF17's activity, resulting in increased activation of its target Rho GTPases. Farnesyl pyrophosphate (FPP) and Geranylgeranyl pyrophosphate (GGPP) serve as substrates for enzymes responsible for the post-translational modification of small GTPases. These lipid attachments are critical for the proper localization and function of GTPases, and ARHGEF17 relies on these modifications to exert its effects efficiently. Thus, the presence of FPP and GGPP can facilitate ARHGEF17-mediated Rho GTPase activation.
Calpeptin acts to inhibit calpain, a protease that can degrade GEFs. This inhibition can help preserve ARHGEF17's structural integrity and functional capacity, ensuring sustained activation of Rho GTPases. Forskolin raises intracellular cAMP levels, which activates protein kinase A (PKA) and can lead to phosphorylation of proteins that interact with ARHGEF17, thus potentially enhancing the GEF activity. Y-27632, a ROCK inhibitor, can indirectly increase GEF activity, as inhibiting ROCK may lead to feedback mechanisms that increase the activity of ARHGEF17 to compensate for reduced active RhoA levels. Compounds like CCG-1423, ML141, CN03, and NSC23766 indirectly influence ARHGEF17 activity by modulating the cellular levels of active Rho GTPases through various mechanisms. For instance, CCG-1423's inhibition of MKL1/SRF-mediated transcription can increase the cellular requirement for active RhoA, while ML141 and CN03 may trigger mechanisms to compensate for the inhibition of Cdc42 and RhoA/B/C, respectively. This can lead to an upregulation of ARHGEF17 activity to restore the balance of active Rho GTPases. Lastly, Gallein's inhibition of Gβγ subunits may result in the enhanced activation of Gα subunits, which can interact with Rho GEFs like ARHGEF17, promoting Rho GTPase activation.
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Guanosine 5′-O-(3-thiotriphosphate) tetralithium salt | 94825-44-2 | sc-202639 | 10 mg | $456.00 | ||
GTPγS is a non-hydrolyzable analog of GTP that binds to G proteins, leading to their persistent activation. Since ARHGEF17 functions as a guanine nucleotide exchange factor (GEF), the presence of GTPγS can enhance the GEF activity of ARHGEF17, resulting in the activation of Rho GTPases. | ||||||
PMA | 16561-29-8 | sc-3576 sc-3576A sc-3576B sc-3576C sc-3576D | 1 mg 5 mg 10 mg 25 mg 100 mg | $40.00 $129.00 $210.00 $490.00 $929.00 | 119 | |
PMA activates protein kinase C (PKC), which can phosphorylate and regulate the activity of several downstream effectors, including Rho GTPases. Through PKC activation, PMA could thus enhance the GEF activity of ARHGEF17 on its Rho GTPase targets. | ||||||
Farnesyl pyrophosphate ammonium salt | 13058-04-3 | sc-200847 sc-200847A | 1 mg 5 mg | $469.00 $1938.00 | ||
FPP is a substrate for protein farnesyltransferase, which modifies and enables proper localization and function of small GTPases. Properly localized and modified GTPases are necessary for ARHGEF17 to exert its GEF activity, thereby activating Rho GTPases. | ||||||
Geranylgeranylpyrophosphate triammonium salt | 6699-20-3 | sc-200849 | 200 µg | $120.00 | ||
GGPP serves as a substrate for protein geranylgeranyltransferase, which, like farnesyltransferase, is necessary for the post-translational modification of small GTPases. GGPP-dependent modifications can facilitate ARHGEF17-mediated activation of Rho GTPases. | ||||||
Calpeptin | 117591-20-5 | sc-202516 sc-202516A | 10 mg 50 mg | $119.00 $447.00 | 28 | |
Calpeptin is a potent inhibitor of calpain, a protease that can cleave and inactivate GEFs. By inhibiting calpain, Calpeptin may prevent the degradation of ARHGEF17, thereby sustaining its activatory function on Rho GTPases. | ||||||
Forskolin | 66575-29-9 | sc-3562 sc-3562A sc-3562B sc-3562C sc-3562D | 5 mg 50 mg 1 g 2 g 5 g | $76.00 $150.00 $725.00 $1385.00 $2050.00 | 73 | |
Forskolin activates adenylate cyclase, increasing cAMP levels, which can enhance PKA activity. PKA can phosphorylate regulatory proteins that interact with ARHGEF17, potentially increasing ARHGEF17 activity on Rho GTPase targets. | ||||||
Y-27632, free base | 146986-50-7 | sc-3536 sc-3536A | 5 mg 50 mg | $182.00 $693.00 | 88 | |
Y-27632 is a ROCK inhibitor that can increase the activity of GEFs indirectly. By inhibiting ROCK, a downstream effector of RhoA, Y-27632 can create feedback that promotes ARHGEF17 GEF activity to replenish active RhoA levels. | ||||||
CCG-1423 | 285986-88-1 | sc-205241 sc-205241A | 1 mg 5 mg | $30.00 $90.00 | 8 | |
CCG-1423 inhibits MKL1/SRF-mediated transcription which is downstream of RhoA signaling. By inhibiting this pathway, CCG-1423 may increase demand for active RhoA, potentially upregulating ARHGEF17 GEF activity to activate RhoA. | ||||||
ML 141 | 71203-35-5 | sc-362768 sc-362768A | 5 mg 25 mg | $134.00 $502.00 | 7 | |
ML141 is a Cdc42 inhibitor. By inhibiting Cdc42, ML141 may trigger compensatory mechanisms to restore active Cdc42 levels, leading to an increase in ARHGEF17 activity to activate Cdc42 through its GEF function. | ||||||
Ro 31-8220 | 138489-18-6 | sc-200619 sc-200619A | 1 mg 5 mg | $90.00 $240.00 | 17 | |
CN03 is a C3 transferase activator that specifically modifies RhoA, B, and C, leading to their inactivation. This modification could stimulate compensatory activation of ARHGEF17 to re-activate these Rho GTPases through its GEF activity. | ||||||