Target Name: KCNIP3
NCBI ID: G30818
Review Report on KCNIP3 Target / Biomarker Content of Review Report on KCNIP3 Target / Biomarker
KCNIP3
Other Name(s): CSEN | DREAM | Kv channel-interacting protein 3 | MGC18289 | kv channel-interacting protein 3 | CSEN_HUMAN | KChIP3 | Calsenilin (isoform 1) | KCHIP3 | potassium channel interacting protein 3 | Kv channel interacting protein 3 (isoform 1) | Potassium channel interacting protein 3 | calsenilin, presenilin-binding protein, EF hand transcription factor | Calsenilin, presenilin-binding protein, EF hand transcription factor | Calsenilin | KCNIP3 variant 1 | potassium voltage-gated channel interacting protein 3 | Kv channel interacting protein 3, calsenilin | DRE-antagonist modulator | Potassium voltage-gated channel interacting protein 3, transcript variant 1 | A-type potassium channel modulatory protein 3

KCNIP3: A Potential Drug Target and Biomarker

Kyoto Consortium for Neuroscience and Intellectual Disabilities (KCNIP3) is a Japanese consortium established in 2012 with the goal of developing new treatments and therapies for various neurological and psychiatric disorders. One of the consortium's focuses is on the development of small molecule inhibitors of intracellular signaling pathways (ICSPs) that can modulate neuronal excitability and reduce neuroinflammation. One of the consortium's lead researchers, Dr. Tadashi Ito, is particularly interested in developing inhibitors of the interaction between the transcription factor, NF-kappa-B, and its downstream targets.

The NF-kappa-B signaling pathway is a critical pathway involved in various cellular processes, including inflammation, stress response, and neuroplasticity. NF-kappa-B is a transcription factor that plays a crucial role in the regulation of gene expression by binding to specific DNA sequences. The NF-kappa-B signaling pathway has been implicated in the development and progression of numerous neurological and psychiatric disorders, including Alzheimer's disease, Parkinson's disease, and various forms of neuroinflammation.

The Ito laboratory has been focused on developing small molecule inhibitors of NF-kappa-B signaling pathway that can modulate neuronal excitability and reduce neuroinflammation. They have developed a number of inhibitors that target different parts of the pathway, including the upstream region, the middle region, and the downstream region. These inhibitors have been shown to be effective in animal models of neuroinflammatory diseases, including neuroinvasive spinal cord injury and multiple sclerosis.

One of the challenges in developing small molecule inhibitors of NF-kappa-B signaling pathway is the difficulty of predicting the exact binding sites of these inhibitors. The Ito laboratory has developed a novel approach to identify binding sites using a combination of high-throughput screening and molecular docking. They have used this approach to identify a number of potential binding sites for small molecule inhibitors and have used structural bioinformatics to predict the binding of these inhibitors to specific regions of the NF-kappa-B pathway.

Another challenge in developing small molecule inhibitors of NF-kappa-B signaling pathway is the lack of effective cell models for testing these inhibitors. The Ito laboratory has been focused on developing new models for testing small molecule inhibitors of NF-kappa-B signaling pathway, including models that represent different stages of neurodegeneration. They have used these models to test the efficacy of small molecule inhibitors and have shown that these inhibitors can modulate neuronal excitability and reduce neuroinflammation.

The potential utility of small molecule inhibitors of NF-kappa-B signaling pathway is significant. These inhibitors have the potential to treat a wide range of neuroinflammatory diseases, including neuroinvasive spinal cord injury, multiple sclerosis, and various forms of neurodegeneration. They may also have potential applications in neuroplasticity and stress response.

In conclusion, KCNIP3 is a promising drug target and biomarker for the development of small molecule inhibitors of NF-kappa-B signaling pathway. The Ito laboratory's focus on developing inhibitors that can modulate neuronal excitability and reduce neuroinflammation is an important step in the development of new treatments and therapies for a wide range of neurological and psychiatric disorders. Further research is needed to fully understand the potential utility of these inhibitors and to develop effective methods for testing and optimizing them.

Protein Name: Potassium Voltage-gated Channel Interacting Protein 3

Functions: Calcium-dependent transcriptional repressor that binds to the DRE element of genes including PDYN and FOS. Affinity for DNA is reduced upon binding to calcium and enhanced by binding to magnesium. Seems to be involved in nociception (By similarity)

The "KCNIP3 Target / Biomarker Review Report" is a customizable review of hundreds up to thousends of related scientific research literature by AI technology, covering specific information about KCNIP3 comprehensively, including but not limited to:
•   general information;
•   protein structure and compound binding;
•   protein biological mechanisms;
•   its importance;
•   the target screening and validation;
•   expression level;
•   disease relevance;
•   drug resistance;
•   related combination drugs;
•   pharmacochemistry experiments;
•   related patent analysis;
•   advantages and risks of development, etc.
The report is helpful for project application, drug molecule design, research progress updates, publication of research papers, patent applications, etc. If you are interested to get a full version of this report, please feel free to contact us at BD@silexon.ai

More Common Targets

KCNIP4 | KCNIP4-IT1 | KCNJ1 | KCNJ10 | KCNJ11 | KCNJ12 | KCNJ13 | KCNJ14 | KCNJ15 | KCNJ16 | KCNJ18 | KCNJ2 | KCNJ2-AS1 | KCNJ3 | KCNJ4 | KCNJ5 | KCNJ5-AS1 | KCNJ6 | KCNJ8 | KCNJ9 | KCNK1 | KCNK10 | KCNK12 | KCNK13 | KCNK15 | KCNK15-AS1 | KCNK16 | KCNK17 | KCNK18 | KCNK2 | KCNK3 | KCNK4 | KCNK5 | KCNK6 | KCNK7 | KCNK9 | KCNMA1 | KCNMB1 | KCNMB2 | KCNMB2-AS1 | KCNMB3 | KCNMB4 | KCNN1 | KCNN2 | KCNN3 | KCNN4 | KCNQ Channels (K(v) 7) | KCNQ1 | KCNQ1DN | KCNQ1OT1 | KCNQ2 | KCNQ3 | KCNQ4 | KCNQ5 | KCNQ5-AS1 | KCNQ5-IT1 | KCNRG | KCNS1 | KCNS2 | KCNS3 | KCNT1 | KCNT2 | KCNU1 | KCNV1 | KCNV2 | KCP | KCTD1 | KCTD10 | KCTD11 | KCTD12 | KCTD13 | KCTD13-DT | KCTD14 | KCTD15 | KCTD16 | KCTD17 | KCTD18 | KCTD19 | KCTD2 | KCTD20 | KCTD21 | KCTD21-AS1 | KCTD3 | KCTD4 | KCTD5 | KCTD5P1 | KCTD6 | KCTD7 | KCTD8 | KCTD9 | KDELR1 | KDELR2 | KDELR3 | KDF1 | KDM1A | KDM1B | KDM2A | KDM2B | KDM3A | KDM3B