Recombinant Human AKAP13 protein, GST-tagged

• Cat.No.: AKAP13-398H
• Product Overview: Recombinant Human AKAP13 protein(NP_001257475.1)(359-587 aa) was fused to GST-tagged and expressed in E. coli.

Specification

• Source: E.coli
• Species: Human
• Tag: GST
• Form: The purified protein was Lyophilized from sterile PBS (58mM Na2HPO4,17mM NaH2PO4, 68mM NaCl, pH7.4). 5% trehalose and 5% mannitol are added as protectants before lyophilization.
• Bio-activity: Not tested
• Protein length: 359-587 aa
• AA Sequence: MIVEEENTDRSCRKKNKGVERKGEE VEPAPIVDSGTVSDQDSCLQSLPDC GVKGTEGLSSCGNRNEETGTKSSGM PTDQESLSSGDAVLQRDLVMEPGTA QYSSGGELGGISTTNVSTPDTAGEM EHGLMNPDATVWKNVLQGGESTKER FENSNIGTAGASDVHVTSKPVDKIS VPNCAPAASSLDGNKPAESSLAFSN EETSTEKTAETETSRSREESADAPV DQNSV
• Endotoxin: Less than 1 EU per ug by the LAL method.
• Purity: 85%, by SDS-PAGE with Coomassie Brilliant Blue staining.
• Applications: Blocking peptide
• Notes: For research use only. Not for use in clinical diagnostic procedures.
• Stability: Store for up to 12 months at -20°C to -80°C as lyophilized powder.
• Storage: Short-term storage: Store at 2-8°C for (1-2 weeks). Long-term storage: Aliquot and store at -20°C to -80°C for up to 3 months, buffer containing 50% glycerol is recommended for reconstitution. Avoid repeat freeze-thaw cycles.
• Reconstitution: It is recommended that sterile water be added to the vial to prepare a stock solution of 0.25 mg/ml. Centrifuge the vial at 4℃ before opening to recover the entire contents.
• Shipping: The product is shipped at ambient temperature. Upon receipt, store it immediately at the recommended temperature (see below).

Gene Information

• Gene Name: AKAP13
• Official Symbol: AKAP13
• Synonyms: BRX; LBC; p47; HA-3; Ht31; c-lbc; PRKA13; AKAP-13; AKAP-Lbc; ARHGEF13; PROTO-LB; PROTO-LBC
• Gene ID: 11214
• mRNA Refseq: NM_001270546.1
• Protein Refseq: NP_001257475.1
• UniProt ID: Q12802

Reviews

05/08/2023

Their team of knowledgeable experts is readily available to address any queries or challenges that may arise during my experiments.

02/01/2020

Its exceptional properties align perfectly with my experimental goals, making it an ideal choice for my scientific investigations.

09/17/2018

In addition to its outstanding quality, the manufacturer provides excellent technical support that has proven to be immensely beneficial.

07/13/2015

This protein showcases exceptional purity and functionality, ensuring robust and reliable outcomes in my research endeavors.

Q&As

Where is AKAP13 found within cells?

AKAP13 is predominantly localized in the cytoplasm, but it can also be found in the membrane structures of cells, including the plasma membrane and intracellular organelles such as the Golgi apparatus. Its precise subcellular localization can vary depending on cell type and specific cellular context.

Is AKAP13 involved in neuronal function?

Yes, AKAP13 has been shown to play a role in neuronal function. It is expressed in various regions of the brain and interacts with key signaling molecules involved in neuronal signaling, including PKA and PKC. AKAP13 has been implicated in neuronal development, synaptic plasticity, and neurotransmitter release. Its dysregulation has been associated with neurodegenerative disorders and psychiatric diseases.

Are there any specific research areas focused on AKAP13?

Research on AKAP13 is diverse and spans various fields, including cell biology, cancer biology, cardiovascular research, and signal transduction. Some specific areas of interest include understanding the molecular mechanisms by which AKAP13 regulates cell migration and invasion, identifying its specific downstream effectors, and exploring its potential as a therapeutic target in specific diseases.

Is AKAP13 expressed in all cell types?

AKAP13 is expressed in various cell types, but its expression levels may vary depending on the cell type and tissue context. It is found in multiple organs, including the heart, brain, liver, and lungs. AKAP13 expression can be regulated by different signaling cues, developmental stages, and disease conditions.

Can AKAP13 be targeted for therapeutic interventions?

While no specific drugs are currently available to directly target AKAP13, ongoing research aims to develop strategies to modulate its activity. The development of small molecule inhibitors or other approaches that disrupt AKAP13 interactions with its binding partners, such as PKA or PKC, may hold potential for therapeutic interventions in diseases where AKAP13 dysregulation contributes to pathogenesis.

Can AKAP13 be regulated by post-translational modifications?

Yes, AKAP13 can be regulated by post-translational modifications. It can undergo phosphorylation by kinases, including PKA and PKC, which can modulate its activity and interactions with other proteins. Additionally, AKAP13 can be subject to other modifications, such as acetylation and SUMOylation, which may also affect its function and cellular localization.

Are there any drugs or therapeutic approaches targeting AKAP13?

Currently, there are no specific drugs targeting AKAP13, but research is ongoing to explore its potential as a therapeutic target. Modulation of AKAP13 activity may provide opportunities for developing novel strategies to treat diseases associated with its dysregulation.

Are there any AKAP13-related animal models?

Yes, AKAP13 knockout mice have been generated to study the physiological functions of AKAP13. These mice have provided valuable insights into the roles of AKAP13 in cardiac hypertrophy and other processes. In addition, gene knockout or knockdown approaches have been used in other model organisms, such as zebrafish and Drosophila, to investigate the functions of AKAP13 homologs in development and disease.

Are there any genetic mutations or polymorphisms associated with AKAP13?

Genetic mutations or polymorphisms in the AKAP13 gene have not been extensively studied. However, some studies have reported associations between certain AKAP13 gene variants and increased cancer risk. More research is needed to determine the specific impact of genetic variations in AKAP13 on disease susceptibility and progression.

How does AKAP13 regulate cAMP/PKA signaling?

AKAP13 acts as a scaffolding protein and plays a crucial role in organizing signaling complexes involved in cAMP/PKA signaling. It binds to the regulatory subunits of PKA and anchors PKA to specific subcellular locations. By doing so, AKAP13 ensures localized activation of PKA in response to cAMP signaling. This allows for precise control of PKA-mediated phosphorylation events and downstream signaling cascades.

What other signaling pathways does AKAP13 regulate?

Besides cAMP/PKA signaling, AKAP13 has been shown to interact with and regulate other signaling pathways. It can modulate the activity of small GTPases, such as RhoA and Rac1, which are involved in various cellular processes, including cytoskeletal dynamics, cell migration, and invasion. AKAP13 also interacts with protein kinase C (PKC) and can influence PKC-mediated signaling. Additionally, AKAP13 has been found to interact with other signaling proteins, such as phosphatidylinositol 3-kinase (PI3K), suggesting its involvement in multiple signaling pathways.

Can AKAP13 be used as a diagnostic or prognostic marker?

Currently, AKAP13 is not widely used as a diagnostic or prognostic marker in clinical practice. However, ongoing research suggests that its altered expression or activity could potentially be used as a marker in specific diseases, such as certain cancers. Further studies are needed to validate its utility in clinical settings.

What are the interacting partners of AKAP13?

AKAP13 interacts with various proteins and signaling molecules. Some of its known interacting partners include PKA, PKC isoforms, small GTPases (such as RhoA and Rac1), phosphatases (such as PP2A), and other scaffolding proteins (such as 14-3-3 proteins). These interactions enable AKAP13 to effectively coordinate multiple signaling pathways.

How is AKAP13 involved in cell migration and invasion?

AKAP13 has been shown to play a crucial role in cell migration and invasion processes. It interacts with small GTPases, such as RhoA and Rac1, which are key regulators of cytoskeletal dynamics and cell movement. AKAP13 promotes the activation of these GTPases by facilitating their recruitment to specific subcellular locations, thereby regulating actin cytoskeleton rearrangement and cell protrusion. This enables cells to migrate and invade through tissues.

Does AKAP13 have any known protein interaction partners?

AKAP13 has several known protein interaction partners. These include regulatory subunits of PKA, PKC isoforms, small GTPases (RhoA and Rac1), phosphatidylinositol 3-kinase (PI3K), and various other signaling proteins and cytoskeletal components. These interactions facilitate the formation of signaling complexes involved in diverse cellular processes.

How is AKAP13 involved in cardiac hypertrophy?

AKAP13 has been shown to play a role in the development of cardiac hypertrophy, a condition characterized by enlargement and thickening of the heart muscle. AKAP13 interacts with protein kinase C (PKC) and mediates its signaling, which is involved in hypertrophic responses. AKAP13 knockout mice have shown reduced cardiac hypertrophy in response to hypertrophic stimuli, suggesting a critical role for AKAP13 in this pathological process.

What diseases or conditions are associated with AKAP13?

AKAP13 dysregulation has been linked to several diseases and conditions. For example, altered expression or activity of AKAP13 has been observed in cardiac hypertrophy, heart failure, and certain types of cancer. In these contexts, AKAP13 may contribute to abnormal cell growth, migration, and survival.