Enzymes
Product List
CAMK2N1 Human
Calcium/Calmodulin Dependent Protein Kinase II Inhibitor 1 Human Recombinant
CAMK2N1 Mouse
Calcium/Calmodulin-Dependent Protein Kinase II Inhibitor 1 Mouse Recombinant
CAMK2N2 Human
Calcium/Calmodulin-Dependent Protein Kinase II Inhibitor 2 Human Recombinant
CAMK4 Human
Calcium/Calmodulin-Dependent Protein Kinase IV Human Recombinant
Introduction
Calcium/Calmodulin-Dependent Protein Kinases (CaMKs) are a family of serine/threonine-specific protein kinases regulated by the calcium-binding messenger protein calmodulin. They play crucial roles in translating calcium signals into cellular responses. The CaMK family includes several isoforms, such as CaMK I, II, III, and IV, each with distinct functions and regulatory mechanisms.
Key Biological Properties: CaMKs are activated by the binding of calmodulin in the presence of calcium ions. This activation leads to autophosphorylation and subsequent phosphorylation of various target proteins.
Expression Patterns: CaMKs are ubiquitously expressed in various tissues, with high expression levels in the brain, heart, and skeletal muscles.
Tissue Distribution:
- CaMK I: Widely distributed but predominantly found in the brain and nervous system.
- CaMK II: Highly expressed in the brain, particularly in the hippocampus, and also present in the heart and skeletal muscles.
- CaMK III: Primarily found in the liver and other metabolic tissues.
- CaMK IV: Expressed in the brain, thymus, and T-cells.
Primary Biological Functions: CaMKs are involved in various cellular processes, including gene expression, cell cycle regulation, and synaptic plasticity. They play a pivotal role in learning and memory by modulating synaptic strength.
Role in Immune Responses: CaMKs are implicated in the regulation of immune cell activation and differentiation. For example, CaMK IV is essential for T-cell activation and cytokine production.
Pathogen Recognition: CaMKs contribute to the immune system’s ability to recognize and respond to pathogens by modulating signaling pathways involved in immune responses.
Mechanisms with Other Molecules and Cells: CaMKs interact with various proteins and cellular structures to exert their effects. They phosphorylate target proteins, leading to changes in their activity, localization, or stability.
Binding Partners: CaMKs bind to calmodulin in a calcium-dependent manner. They also interact with other proteins, such as transcription factors, ion channels, and cytoskeletal proteins.
Downstream Signaling Cascades: Upon activation, CaMKs initiate a cascade of phosphorylation events that propagate the calcium signal. This can lead to the activation of transcription factors, changes in gene expression, and alterations in cellular functions.
Expression and Activity Control: The expression and activity of CaMKs are tightly regulated at multiple levels, including transcriptional, post-transcriptional, and post-translational mechanisms.
Transcriptional Regulation: The expression of CaMK genes is regulated by various transcription factors and signaling pathways. For example, CaMK IV expression is controlled by the cAMP response element-binding protein (CREB).
Post-Translational Modifications: CaMKs undergo several post-translational modifications, such as phosphorylation, ubiquitination, and sumoylation, which modulate their activity, stability, and interactions with other proteins.
Biomedical Research: CaMKs are extensively studied in the context of neurological disorders, cardiovascular diseases, and cancer. They serve as valuable models for understanding calcium signaling and its implications in health and disease.
Diagnostic Tools: Alterations in CaMK activity or expression can serve as biomarkers for certain diseases. For example, elevated CaMK II activity is associated with cardiac hypertrophy and heart failure.
Therapeutic Strategies: Targeting CaMKs with specific inhibitors or modulators holds potential for treating various conditions, such as neurodegenerative diseases, cardiac disorders, and immune-related diseases.
Development: CaMKs play critical roles in embryonic development, particularly in the formation and maturation of the nervous system.
Aging: Changes in CaMK activity are associated with aging-related processes, such as cognitive decline and muscle atrophy.
Disease: Dysregulation of CaMK signaling is implicated in various diseases, including Alzheimer’s disease, Parkinson’s disease, heart failure, and autoimmune disorders.
