Recombinant Human ARHGEF12 293 Cell Lysate

• Cat.No.: ARHGEF12-8734HCL

Specification

• Description: Antigen standard for Rho guanine nucleotide exchange factor (GEF) 12 (ARHGEF12) is a lysate prepared from HEK293T cells transiently transfected with a TrueORF gene-carrying pCMV plasmid and then lysed in RIPA Buffer. Protein concentration was determined using a colorimetric assay. The antigen control carries a C-terminal Myc/DDK tag for detection.
• Source: HEK 293 cells
• Species: Human
• Components: This product includes 3 vials: 1 vial of gene-specific cell lysate, 1 vial of control vector cell lysate, and 1 vial of loading buffer. Each lysate vial contains 0.1 mg lysate in 0.1 ml (1 mg/ml) of RIPA Buffer (50 mM Tris-HCl pH7.5, 250 mM NaCl, 5 mM EDTA, 50 mM NaF, 1% NP40). The loading buffer vial contains 0.5 ml 2X SDS Loading Buffer (125 mM Tris-Cl, pH6.8, 10% glycerol, 4% SDS, 0.002% Bromophenol blue, 5% beta-mercaptoethanol).
• Size: 0.1 mg
• Storage Instruction: Store at -80°C. Minimize freeze-thaw cycles. After addition of 2X SDS Loading Buffer, the lysates can be stored at -20°C. Product is guaranteed 6 months from the date of shipment.
• Applications: ELISA, WB, IP. WB: Mix equal volume of lysates with 2X SDS Loading Buffer. Boil the mixture for 10 min before loading (for membrane protein lysates, incubate the mixture at room temperature for 30 min). Load 5 ug lysate per lane.

Gene Information

• Gene Name: ARHGEF12 Rho guanine nucleotide exchange factor (GEF) 12 [ Homo sapiens ]
• Official Symbol: ARHGEF12
• Synonyms: ARHGEF12; Rho guanine nucleotide exchange factor (GEF) 12; rho guanine nucleotide exchange factor 12; KIAA0382; LARG; leukemia-associated RhoGEF; leukemia-associated rho guanine nucleotide exchange factor; PRO2792; DKFZp686O2372
• Gene ID: 23365
• mRNA Refseq: NM_001198665
• Protein Refseq: NP_001185594
• MIM: 604763
• UniProt ID: Q9NZN5
• Chromosome Location: 11q23.3
• Pathway: Axon guidance, organism-specific biosystem; Axon guidance, conserved biosystem; Axon guidance, organism-specific biosystem; Cell death signalling via NRAGE, NRIF and NADE, organism-specific biosystem; Developmental Biology, organism-specific biosystem; G alpha (12/13) signalling events, organism-specific biosystem; GPCR downstream signaling, organism-specific biosystem
• Function: G-protein coupled receptor binding; GTPase activator activity; Rho guanyl-nucleotide exchange factor activity; guanyl-nucleotide exchange factor activity

Reviews

07/26/2022

ARHGEF12 protein is highly recommended for use in various research applications, including ELISA and protein electron microscopy structure analysis.

04/23/2019

Their knowledgeable and responsive team of experts is readily available to provide guidance, troubleshooting assistance, and answer any inquiries or concerns I may have.

01/05/2019

They ensure a reliable and consistent supply of ARHGEF12 protein, minimizing any potential disruptions in my experimental workflow.

03/07/2018

The ARHGEF12 protein offers exceptional quality that meets the rigorous demands of experimental research.

01/28/2018

Whether it involves experimental design, protocol optimization, or data analysis, their expertise can help me navigate through complexities, saving valuable time and resources.

01/22/2017

They ensure a reliable and consistent supply of ARHGEF12 protein, minimizing any potential disruptions in my experimental workflow.

05/12/2016

ARHGEF12 protein's utility extends to protein electron microscopy structure analysis, where it plays a crucial role in investigating the detailed architecture and conformational changes of proteins.

03/11/2016

It exhibits exceptional performance in ELISA assays, making it an excellent choice for researchers studying angiopoietins, angiogenesis, or vascular biology.

Q&As

Are there any animal models available to study ARHGEF12 function?

Yes, animal models such as mice have been used to study ARHGEF12 function. Knockout mouse models, where the ARHGEF12 gene is disrupted or deleted, have been generated to investigate the physiological and behavioral consequences of its loss. These models can provide insights into the role of ARHGEF12 in development, neurological processes, and disease.

Can targeting ARHGEF12 have therapeutic potential?

Yes, targeting ARHGEF12 has the potential for therapeutic intervention. Since dysregulation of ARHGEF12 contributes to cancer progression and metastasis, inhibiting its activity could impede these processes. Furthermore, understanding the role of ARHGEF12 in other diseases, such as cardiovascular disorders, may pave the way for developing novel therapeutic strategies.

Are there any known interacting proteins or molecular partners of ARHGEF12?

Yes, ARHGEF12 can interact with a variety of proteins and molecules. For example, it can interact with certain Rho GTPases, such as RhoA and Rac1, to regulate their activation. ARHGEF12 can also associate with other signaling proteins, adaptor molecules, and cytoskeletal components to mediate its cellular functions.

Are there any diseases or disorders associated with dysregulation of ARHGEF12 expression or activity?

Yes, dysregulation of ARHGEF12 has been implicated in several diseases. For example, alterations in ARHGEF12 expression have been observed in certain cancers, such as breast, lung, and colorectal cancers. Dysregulation of ARHGEF12 can contribute to tumor progression and metastasis by promoting cellular processes like migration and invasion.

Can ARHGEF12 be targeted for therapeutic purposes?

The potential therapeutic targeting of ARHGEF12 is an area of ongoing research. Since ARHGEF12 is involved in various cellular processes and implicated in certain diseases, it represents a potential target for therapeutic intervention. However, further investigation is needed to understand its precise role in disease mechanisms and develop effective therapeutic strategies.

Can ARHGEF12 be regulated by post-translational modifications?

Yes, post-translational modifications can regulate the activity and function of ARHGEF12. For instance, phosphorylation of specific sites on ARHGEF12 can modulate its activity and interaction with other proteins. Other post-translational modifications, such as acetylation, methylation, and ubiquitination, may also play a role in regulating ARHGEF12. These modifications can impact its stability, localization, and interaction with signaling partners.

How does ARHGEF12 regulate Rho GTPases?

ARHGEF12 facilitates the exchange of GDP (guanosine diphosphate) for GTP (guanosine triphosphate) on Rho GTPases. This GTP binding leads to the activation of Rho GTPases, allowing them to interact with downstream effectors and regulate cytoskeletal dynamics and other cellular functions.

Are there any drugs or compounds that target ARHGEF12?

Currently, there are no specific drugs or compounds that directly target ARHGEF12. However, there are drugs that indirectly modulate the activity or downstream effects of Rho GTPases, which can indirectly affect ARHGEF12 signaling. For example, inhibitors of Rho-associated protein kinases (ROCKs), which are downstream effectors of RhoA, can impact the cellular processes influenced by ARHGEF12. Additionally, compounds targeting other pathways that intersect with ARHGEF12-mediated signaling, such as inhibitors of signaling pathways associated with cancer metastasis, may indirectly affect ARHGEF12 activity.

Is ARHGEF12 involved in neuronal development or synaptic plasticity?

Yes, ARHGEF12 plays a role in neuronal development and synaptic plasticity. It has been found to be involved in the regulation of dendritic spine morphology, synapse formation, and axon guidance. Disruptions in ARHGEF12 function can impact these processes, potentially leading to neurological disorders.

Are there any known genetic mutations or variations in the ARHGEF12 gene?

Yes, genetic variations and mutations have been identified in the ARHGEF12 gene. Some of these variations have been associated with certain diseases or disorders. For example, a specific mutation in the ARHGEF12 gene has been linked to familial juvenile myoclonic epilepsy (JME), a type of seizure disorder.

How does ARHGEF12 contribute to cancer progression?

ARHGEF12 can contribute to cancer progression through its effects on cell migration, invasion, and metastasis. Dysregulation of ARHGEF12 can lead to aberrant cytoskeletal remodeling, promoting the invasive behavior of cancer cells. In addition, studies have shown that ARHGEF12-mediated signaling can activate downstream pathways involved in cell survival, proliferation, and angiogenesis, which are important for tumor growth and metastasis. These findings suggest that ARHGEF12 may be a potential therapeutic target for inhibiting cancer progression.

Are there any known inhibitors or activators of ARHGEF12?

Yes, a few compounds have been identified as regulators of ARHGEF12 activity. For instance, Ipatasertib, a small molecule inhibitor, can inhibit the activity of ARHGEF12. Additionally, ARHGEF12 can be activated by various signals, including protein kinases like PKD1, which phosphorylates and activates ARHGEF12, leading to Rho GTPase activation.

Does ARHGEF12 have any known roles in immune responses?

While ARHGEF12's role in immune responses is less well-studied compared to other cellular processes, emerging evidence suggests its involvement in immune cell migration and activation. ARHGEF12 has been shown to regulate cytoskeletal remodeling in immune cells, which can impact their ability to migrate and respond to stimuli. Further research is needed to fully elucidate its role in immune responses.

Has ARHGEF12 been implicated in any human diseases?

Yes, ARHGEF12 has been implicated in several human diseases and disorders. For instance, mutations or variations in the ARHGEF12 gene have been associated with familial juvenile myoclonic epilepsy (JME). ARHGEF12 has also been implicated in the progression of certain types of cancer, including colorectal cancer and breast cancer. Its dysregulation has been linked to aberrant cytoskeletal dynamics and invasive behavior in cancer cells.

How is ARHGEF12 involved in cytoskeletal remodeling?

ARHGEF12 plays a crucial role in cytoskeletal remodeling through its activation of Rho GTPases, particularly RhoA and Rac1. ARHGEF12 acts as a guanine nucleotide exchange factor (GEF), facilitating the exchange of GDP (inactive form) for GTP (active form) on Rho GTPases. This activation leads to downstream signaling cascades that regulate actin polymerization, cell adhesion, and cell migration. By modulating the activity of Rho GTPases, ARHGEF12 can influence the organization and dynamics of the cytoskeleton.

Are there any ongoing clinical trials involving ARHGEF12?

As of now, there are no ongoing clinical trials specifically targeting ARHGEF12. However, this may change in the future as more research uncovers its potential therapeutic relevance in diseases such as epilepsy and cancer. It is always recommended to regularly check clinical trial databases for updates on ARHGEF12-related trials.

Is ARHGEF12 expressed in all tissues?

ARHGEF12 is broadly expressed in various tissues and cell types. Its expression levels can vary depending on the specific tissue and developmental stage. Higher expression levels of ARHGEF12 are often detected in tissues with high actin remodeling, such as the brain, heart, skeletal muscle, and immune cells. However, it is important to note that expression patterns can vary depending on the specific physiological or pathological context.