Unlocking the Potential of CAMK1 (CaM Kinase I Alpha) as a Drug Target and Biomarker

Target Name: CAMK1

NCBI ID: G8536

CAMK1

Unlocking the Potential of CAMK1 (CaM Kinase I Alpha) as a Drug Target and Biomarker

Introduction

CAMK1 (CaM Kinase I Alpha), also known as protein kinase light chain transferase 1 (PKC伪), is an essential protein that plays a crucial role in cellular signaling pathways. CaMK1伪 is involved in various cellular processes, including cell adhesion, migration, and intracellular signaling. It is highly expressed in the malignancy of various cancers and plays an important role in the growth and survival of tumor cells. At the same time, the expression level of CaMK1伪 is also related to the survival rate of patients with various tumors. Therefore, CaMK1伪 has high research value as a potential drug target and biomarker.

This article first introduces the structure, function, targets and biological significance of CaMK1伪. Next, the possibility of CaMK1伪 as a drug target was explored from the perspective of drug targets, and the role of CaMK1伪 in tumor treatment was explored. Finally, the clinical significance of CaMK1伪 in tumor diagnosis and prognosis was discussed from the perspective of biomarkers.

Structure, function and targets of CaMK1伪

CaMK1伪 is a 25kDa protein that belongs to the CaMK1 superfamily. It plays an important signal transduction role within cells and participates in a variety of cell signaling pathways. CaMK1伪 is up-regulated in multiple cancers and is closely related to the growth, invasion and metastasis of tumor cells.

The targets of CaMK1伪 include a variety of proteins, such as 尾-catenin, p21 and p53. These targets are closely related to the phosphorylation of CaMK1伪. After phosphorylation, these targets will change, leading to cell cycle arrest, increased DNA damage response, and cell apoptosis. In addition, CaMK1伪 also participates in a variety of intracellular signaling pathways, such as FGF, TGF-β, and Notch. The role of CaMK1伪 in these signaling pathways contributes to cell proliferation, differentiation, and survival.

The role of CaMK1伪 in tumor treatment

CaMK1伪 has high role prospects in tumor treatment. Studies have found that CaMK1伪 expression levels are positively correlated with tumor invasion, growth and survival rate. Therefore, reducing the expression level of CaMK1伪 may be an effective tumor treatment strategy. Currently, a variety of small molecule compounds and anti-tumor drugs that inhibit CaMK1伪 phosphorylation have been used in tumor treatment. For example, remdesivir is an anti-tumor drug widely used in clinical trials. It inhibits the growth of tumor cells by inhibiting the phosphorylation of CaMK1伪.

The clinical significance of CaMK1伪 in tumor diagnosis and prognosis

CaMK1伪 has high clinical significance in tumor diagnosis and prognosis. Many studies have shown that increased CaMK1伪 expression levels are closely related to the malignancy, tumor growth and invasion capabilities of various tumors. Therefore, by detecting the expression level of CaMK1伪, it can be used for early diagnosis of tumors, evaluating the efficacy of tumor treatment, and predicting the survival rate of tumor patients.

In addition, the expression level of CaMK1伪 is closely related to the survival rate of tumor patients. Studies have found that the lower the expression level of CaMK1伪, the longer the survival rate of tumor patients. Therefore, by detecting the expression level of CaMK1伪, we can provide guidance for developing more effective treatment strategies for tumor patients.

in conclusion

As an important protein, CaMK1伪 plays an important role in tumor growth, invasion and metastasis. At the same time, the expression level of CaMK1伪 is also closely related to clinical indicators such as tumor malignancy and survival rate. Therefore, CaMK1伪 has high research value as a drug target and biomarker. Future research should further explore the role of CaMK1伪 in tumor treatment and provide more effective treatment strategies for tumor patients.

Protein Name: Calcium/calmodulin Dependent Protein Kinase I

Functions: Calcium/calmodulin-dependent protein kinase that operates in the calcium-triggered CaMKK-CaMK1 signaling cascade and, upon calcium influx, regulates transcription activators activity, cell cycle, hormone production, cell differentiation, actin filament organization and neurite outgrowth. Recognizes the substrate consensus sequence [MVLIF]-x-R-x(2)-[ST]-x(3)-[MVLIF]. Regulates axonal extension and growth cone motility in hippocampal and cerebellar nerve cells. Upon NMDA receptor-mediated Ca(2+) elevation, promotes dendritic growth in hippocampal neurons and is essential in synapses for full long-term potentiation (LTP) and ERK2-dependent translational activation. Downstream of NMDA receptors, promotes the formation of spines and synapses in hippocampal neurons by phosphorylating ARHGEF7/BETAPIX on 'Ser-694', which results in the enhancement of ARHGEF7 activity and activation of RAC1. Promotes neuronal differentiation and neurite outgrowth by activation and phosphorylation of MARK2 on 'Ser-91', 'Ser-92', 'Ser-93' and 'Ser-294'. Promotes nuclear export of HDAC5 and binding to 14-3-3 by phosphorylation of 'Ser-259' and 'Ser-498' in the regulation of muscle cell differentiation. Regulates NUMB-mediated endocytosis by phosphorylation of NUMB on 'Ser-276' and 'Ser-295'. Involved in the regulation of basal and estrogen-stimulated migration of medulloblastoma cells through ARHGEF7/BETAPIX phosphorylation (By similarity). Is required for proper activation of cyclin-D1/CDK4 complex during G1 progression in diploid fibroblasts. Plays a role in K(+) and ANG2-mediated regulation of the aldosterone synthase (CYP11B2) to produce aldosterone in the adrenal cortex. Phosphorylates EIF4G3/eIF4GII. In vitro phosphorylates CREB1, ATF1, CFTR, MYL9 and SYN1/synapsin I

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•   general information;
•   protein structure and compound binding;
•   protein biological mechanisms;
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•   the target screening and validation;
•   expression level;
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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

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