IQGAP1 (IQ motif containing GTPase activating protein 1) is a [[scaffold]]ing protein that is highly conserved across species and is widely expressed in various tissues. It has been shown to play a critical role in many cellular processes, including [[cell adhesion]], migration, proliferation, and differentiation.

IQGAP1 contains multiple domains, including IQ motifs that can bind to [[calmodulin]] and Ras GTPases, a WW domain that binds to proline-rich motifs, and a C-terminal domain that interacts with actin filaments. Through these interactions, IQGAP1 can modulate the activity of various signaling pathways, such as the Rho GTPase and MAPK pathways, and regulate the organization and dynamics of the actin [[cytoskeleton]].

Studies have suggested that IQGAP1 is involved in the development and progression of several human diseases, including [[cancer]], cardiovascular disease, and neurological disorders. Dysregulation of IQGAP1 expression and activity has been implicated in tumor invasion and metastasis, as well as in the pathogenesis of [[Alzheimer's disease]] and stroke.

Given its multifaceted roles in cellular physiology and pathology, IQGAP1 is an important subject of research in the fields of cell biology, cancer biology, and neuroscience.
----
[[Diffuse]] invasion is an important factor leading to treatment [[resistance]] and a poor [[prognosis]] in [[glioma]]s. 
Zhang et al. found that [[expression]] of the tripartite motif containing 56 ([[TRIM56]]), a [[RING-finger domain]] containing [[E3 ubiquitin ligase]], was markedly higher in glioma than in normal brain tissue, and was significantly correlated with malignant [[phenotype]]s and a poor [[prognosis]]. [[In vitro]] and in vivo experimental studies revealed that TRIM56 promoted the migration and invasion of [[glioma cell]]s. Mechanistically, TRIM56 was transcriptionally regulated by [[SP1]] and promoted the K48-K63-linked poly-ubiquitination transition of [[IQGAP1]] at Lys-1230 by interacting with it, which in turn promoted [[CDC42]] activation. This mechanism was confirmed to mediate glioma migration and invasion. 

The study provides insights into the mechanisms through which TRIM56 promotes glioma motility, i.e., by regulating IQGAP1 ubiquitination to promote CDC42 activation, which might be clinically targeted for the treatment of glioma
((Zhang Q, Zheng J, Wu W, Lian H, Iranzad N, Wang E, Yang L, Wang X, Jiang X. TRIM56 acts through the IQGAP1-CDC42 signaling axis to promote glioma cell migration and invasion. Cell Death Dis. 2023 Mar 4;14(3):178. doi: 10.1038/s41419-023-05702-6. PMID: 36870986.)).