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- Table of Contents
Facts about Ras GTPase-activating-like protein IQGAP1.
It partners with calmodulin. Could function as a meeting scaffold for the organization of a multimolecular complex that would interface incoming signals to the reorganization of the actin cytoskeleton in the plasma membrane.
Human | |
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Gene Name: | IQGAP1 |
Uniprot: | P46940 |
Entrez: | 8826 |
Belongs to: |
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No superfamily |
HUMORFA01; IQ motif containing GTPase activating protein 1; IQGAP1; KIAA0051ras GTPase-activating-like protein IQGAP1; p195; p195RasGAP-like with IQ motifs; SAR1
Mass (kDA):
189.252 kDA
Human | |
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Location: | 15q26.1 |
Sequence: | 15; NC_000015.10 (90388242..90502239) |
Expressed in the placenta, lung, and kidney. A lower level expression is seen in the heart, liver, skeletal muscle and pancreas.
Cell membrane. Nucleus. Cytoplasm. Subcellular distribution is regulated by the cell cycle, nuclear levels increase at G1/S phase (PubMed:20883816).
IQGAP1 is an inter-functional scaffold protein. It regulates the growth and invasion of tumor cells. It is a unique antigen for cancer. Boster Bio developed a reagent that detects IQGAP1 through monoclonal or polyclonal antigens. This product is highly versatile and can be utilized for a variety of uses. We will look at its most commonly used uses and how it can be utilized for clinical diagnostics and research.
The IQ domain of IQGAP1 shows a homology of the domain to the calponin. In this study, IQGAP1 is found to interact with the Ras GTPase, Nrf2, and it binds to its His-tagged counterpart. The amino acid residues 699-905 in IQGAP1 are the IQ domain.
In myeloma cells, IQGAP1 is overexpressed and regulates MAPK signals. The SP1/p300 complex is the upstream regulator for IQGAP1. IQGAP1 promotes the interaction between Akt and mTOR, which results in increased Akt activation.
While IQGAP1 interacts with a variety of signaling molecules, the exact mechanism through which it binds to Ras is not clear. Various approaches have been proposed to disrupt the Ras-binding proteins, and various approaches have been devised to achieve this. BioGRID compiles published literature about Ras-IQGAP1 interactions. STRING does not correctly state, however, that all Ras isoforms can be IQGAP1 binding members.
Different extracellular signals trigger the ERK MAPK pathway, such as EGF, IGF-1, NGF, and PDGF. Inhibition of IQGAP1 through one of these extracellular signals induces different outputs in the cells. One of these is differentiation, and the other is the proliferation. The IQGAP1 protein is thought to be responsible for EGF's specific output.
The results indicated that IQGAP1 inhibits MEKERK-mediated enhanced stability of Nrf2. Further, knockdown of IQGAP1 attenuated the MEK-ERK-Nrf2 signaling pathway and reduced the expression of phase II detoxifying/antioxidant genes in HEK-293 cells. In addition, the knockdown of IQGAP1 slowed MEK-ERK-induced increased nuclear translocation of Nrf2, whereas IQGAP1-knockdown cells decreased ubiquitination of Nrf2 in comparison to wild-type cells.
The IQGAP1 protein is still involved in its intrinsic regulatory function in secretion, and regulates the flow of protein. IQGAP1's negative control of secretory lysosome transport towards the plasma membrane and its inhibition of agonist-stimulated histamine secretion from mast cells is another reason. The IQGAP1 protein also functions as a marker of position for budding yeast, directing the exocytic secretion pathway towards the buds' site or cytokinetic plate.
IQGAP1 regulates a variety of key molecules via its multi-functional scaffold protein. Its IQ domain is composed of four tandem IQ motif. It is also involved in interactions with the calmodulin protein that regulates a variety of target proteins. It interacts with protein kinases and cell surface receptors. It also triggers MAPK signaling. These interactions permit IQGAP1 block carcinogenesis.
The IQGAP family of scaffold proteins has three members, each has distinct roles in HCC and liver illnesses. Because they are involved in various signaling pathways, IQGAPs could be a promising therapeutic target for HCC. IQGAP1 plays different roles in primary and secondary HCC, hepatic fibrosis, and liver the fibrosis. IQGAP3 is critical for liver regeneration after injury.
Research on RNA interference was conducted to determine the function of IQGAP1. The siRNA was synthesized by RiboBio Co. Ltd., Guangzhou, China. The sequence of siRNA against IQGAP1 was 5'-UUA CCC AGA AUC UUG G-3", and the negative control oligonucleotides contained 5'-UA CCC GUA CGU ACG'. Cell suspensions were evaluated by flow cytometry.
IQGAP1 is an essential structural component of IQGAPs. It also interacts with a variety of proteins to regulate cell signaling. This is a wide range of functions in carcinogenesis. IQGAP1 directly interacts with RhoA/C, acting as a pro-oncogenic factor in breast cancer. It binds to b-catenin that is a protein involved in the development of liver cancer. It also interacts with CDC42 which plays a role in oncogenic transformation and invasion.
IQGAP1 plays a crucial role in osteoblast and bone marrow growth. Ma and colleagues have demonstrated that S1P induces membrane translocation of IQGAP1 as well as enhances its interaction with Cdc42/Rac1, which results in increased movement of BMSCs. Interestingly, knockdown of IQGAP1 significantly decreased BMSC cell viability and migration capacity.
A variety of cancers have the IQGAP1 gene in their cells. These cells exhibit invasive behavior that is closely related to the presence of the IQGAP1–RAC1. The complex regulates the activation of actin and phosphorylates the ERK2 enzyme and contributes to the growth of tumors. Recent research has shown that IQGAP1 levels are greater in CSC-LCs which have increased invasion properties. IQGAP1 could therefore play a role in the metastasis of ovarian cancer.
IQGAPs that are evolutionarily conserved proteins, are found in eukaryotic cells. They have three closely related homologs and regulate many biological processes. A lack of IQGAP1 expression is associated with poor clinical outcomes and a higher chance of recurrence among various types of cancer. IQGAP1 regulates cancer cell proliferation and invasion in two ways: by enhancing adhesion between cells and by facilitating cell-cell interactions.
IQGAP1's activity is thought to involve the capture of microtubule ends and forming tripartite compounds using activated Cdc42. It also plays a role in the formation podosomes, that resemble invadopodia. The IQGAP1T gene is active in a constant manner, and requires the Cterminal domain of CLIP170/adenomatous Polyposis coli.
IQGAP1 plays a significant role in the development and spread of HNSCC. This protein is crucial for normal development and growth of cancer cells, since it regulates the JNK pathway. The findings of the study are promising and suggest that there is a more effective treatment option for HNSCC. However it is imperative to conduct further research before it becomes possible to implement new treatment strategies. With further research we can develop an understanding of the tumor cells and their ability to invade.
IQGAP1 is a cancer antigen that is linked to immune responses that are related to tumors. IQGAP1 could play an important role in tumor immunology and could prove to be a useful target for the development of new anti-tumor therapies. This article gives a brief overview of the possible applications of IQGAP1. This article will highlight the key benefits of targeting this cancer antigen.
Researchers used immunoprecipitation to determine IQGAP1 levels that are specific to tumors. The authors used a polyhydroxyethylmethacrylate-coated 6-well cell culture dish to identify tumor cells. Both proteins were expressed at low levels and showed similar distribution patterns. Both proteins displayed similar expression patterns in breast cancer. For instance when SASh2 is expressed at low levels, IQGAP1 expression is increased, and vice versa.
In mice, IQGAP1 knockdown increased myofibroblastic activation (HSCs) in mice. The survival of coimplanted HSCs was assessed by in vivo xenogen-based imaging. Mice were implanted with TbRIIHA-tagged HSCs or the HT29 tumor cells. Bioluminescence decreased in a continuous manner over the period of days 6, 14 and 23 following implant. However, it was still visible at the time of day 23 for mice co-implanted with tumor cells.
IQGAP1 is associated with TbRII. Knockdown of IQGAP1 in mice did not alter the mRNA level of TbRII. IQGAP1 and TbRII were colocalized at the plasma membrane as well as within the arrowheads. They also coimmunoprecipitated the endogenous TbRII.
IQGAP1 reduces activity in myofibroblasts derived from tumors. It also inhibits the synthesis of TbRII and, consequently, inhibits the proliferation of tumor cells. Therefore, the ability of this antigen to prevent the growth of liver cancer can greatly assist in the development of new treatments against colorectal cancer. The IQGAP1 gene is also reduced in colorectal liver metastases.
The IQGAP1 gene encodes one of the IQGAP family. The protein is composed of four IQ domains. It is also linked with the calponindomain, Ras-GAPdomain, as well as the WW domain. It regulates cell morphology and interacts with cell adhesion molecules. The increase in this protein's expression has been associated with the amplification of genes.
PMID: 8051149 by Weissbach L., et al. Identification of a human rasGAP-related protein containing calmodulin-binding motifs.
PMID: 15355962 by Grohmanova K., et al. Phosphorylation of IQGAP1 modulates its binding to Cdc42, revealing a new type of rho-GTPase regulator.