Human ARHGAP18 blocking peptide (CDBP0473)

Synthetic Human ARHGAP18 blocking peptide for BL

Product Overview
Blocking peptide for anti-ARHGAP18 antibody
Species Reactivity
Application Notes
For in vitro research use only. Not intended for any diagnostic or therapeutic purpose. Not suitable for human or animal consumption.
200 μg/ml
50 μg
PBS containing 0.02% sodium azide
0.02% Sodium Azide
Store at -20℃, stable for one year.
UniProt ID
Antigen Description
ARHGAP18 belongs to a family of Rho (see MIM 165390) GTPase-activating proteins that modulate cell signaling (Potkin et al., 2009 [PubMed 19065146]).[supplied by OMIM, Apr 2010]
GTPase activator activity;
ARHGAP18; Rho GTPase activating protein 18; SENEX; MacGAP; bA307O14.2; rho GTPase-activating protein 18; rho-type GTPase-activating protein 18;


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The RhoA Gtpase Activating Protein ARHGAP18 Regulates Mesenchymal Stem Cell Lineage Commitment


Authors: Yen, Sherwin S.; Thompson, William R.; Uzer, Gunes; Xie, Zhihui; Sen, Buer; Styner, Maya; Burridge, Keith; Rubin, Janet E.

Activation of human gonadotropin-releasing hormone receptor promotes down regulation of ARHGAP18 and regulates the cell invasion of MDA-MB-231 cells


Authors: Aguilar-Rojas, Arturo; Maya-Nunez, Guadalupe; Huerta-Reyes, Maira; Perez-Solis, Marco Allan; Silva-Garcia, Raul; Guillen, Nancy; Olivo-Marin, Jean-Christophe

The Gonadotropin-Releasing Hormone Receptor (GnRHR) is expressed mainly in the gonadotrope membrane of the adenohypophysis and its natural ligand, the Gonadotropin-Releasing Hormone (GnRH), is produced in anterior hypothalamus. Furthermore, both molecules are also present in the membrane of cells derived from other reproductive tissues such as the breast, endometrium, ovary, and prostate, as well as in tumors derived from these tissues. The functions of GnRH receptor and its hormone in malignant cells have been related with the decrease of proliferation and the invasiveness of those tumors however, little is known about the molecules associated with the signaling pathways regulated by both molecules in malignant cells. To further analyze the potential mechanisms employed by the GnRHR/GnRH system to reduce the tumorigenesis of the highly invasive breast cancer cell line MDA-MB-231, we performed microarrays experiments to evaluated changes in genes expression and validate these modifications by functional assays. We show that activation of human GnRHR is able to diminish the expression and therefore functions of the Rho GTPase-Activating Protein 18 (ARHGAP18). Decrease of this GAP following GnRHR activation, correlates to the higher of cell adhesion and also with reduction of tumor cell invasion, supporting the notion that GnRHR triggers intracellular signaling pathways that acts through ARHGAP18. On the contrary, although a decline of cellular proliferation was observed during GnRHR activation in MDA-MB-231, this was independent of ARHGAPI8 showing the complex system in which is involved the signaling pathways regulated by the GnRHR/GnRH system. (C) 2017 Elsevier B.V. All rights reserved.

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