MAP3K5

What is MAP3K5 protein?

Mitogen-Activated Protein Kinase Kinase Kinase 5, or MAP3K5 protein for short, this particular protein carries an array of responsibilities in several critical cellular processes. The discovery of MAP3K5 dates back to studies undertaken in the early 1990s where it was found to be among the family of serine/threonine-protein kinases and is encoded by the MAP3K5 gene. Conserved across several species, MAP3K5 is scientifically recognized as MKK Kinase, sometimes referred to as Apoptosis Signal-regulating Kinase 1 (ASK1) due to its essential role in cellular death processes.

The MAP3K5 gene in humans is found on the chromosome 6, precisely at the locus 6q22.33 which highlights the physical and genetic position of where the protein does originate from an individual's genetic makeup.

Protein Structure

The MAP3K5 protein structure comprises several functional domains. It includes a C-terminal region with an important kinase domain that contains a catalytic core structure typical of serine/threonine-protein kinases. Notably, it also includes a serine-rich region associated with regulatory phosphorylation sites, N-terminal domain holds a protein-protein interaction domain coiled-coil, and a nuclear export signal (NES) and nuclear localization signal (NLS) sequences.

What are the functions of MAP3K5 protein?

Functionally, MAP3K5 protein engages in various processes driving essential functions of life in living organisms. This protein acts as a nodal point in the MAPK signaling pathway, receiving signals from various receptors and delivering them to downstream effectors. It activates two main subfamilies of MAP2Ks: MKK4/MKK7 (which activate JNK pathway) and MKK3/MKK6 (which activate the p38 pathways).

MAP3K5 protein plays a crucial role in numerous physiological processes ranging from apoptosis, inflammation, response to oxidative stress, cell differentiation to immune response. This protein is pivotal in mediating apoptosis (programmed cell death), a vital process in human health and disease. During oxidative stress, MAP3K5 is activated, leading to apoptosis for the preservation of organismic integrity.

MAP3K5 Protein Related Signal Pathway

The MAP3K5 protein plays a critical role in the MAPK signaling pathway. The Mitogen-activated protein kinase (MAPK) pathway is a biochemical route in the cell that transmits information from the cell surface to the DNA in the nucleus, ultimately influencing genetic activity. The MAPK pathways are vital for various cellular functions including survival, proliferation, differentiation, and apoptosis.

MAP3K5 protein, as a component of the MAPK signaling pathway, functions at the upstream level where it receives and processes signals before transmitting them to downstream components. The protein is involved in the activation of both the p38 MAPK and the JNK MAP kinase pathways.

MAP3K5 Protein Related Diseases

utation or deviation from normal functionality of MAP3K5 protein has links with several diseases. Given its central role in a variety of physiological processes, abnormalities in the MAP3K5 protein can lead to complexities. Evidence suggests it in the pathophysiology of neurodegenerative diseases like Alzheimer's and Parkinson's disease. In Alzheimer's disease, for example, the role of MAP3K5 protein in neuronal death presents the possibility of it being a potential therapeutic target.

Additionally, aberrations in the MAP3K5 protein and its pathways have been implicated in cancer biology. Studies have shown that MAP3K5 protein might endorse tumor growth in certain types of cancer, such as lung and breast cancer. Notably, more studies are needed in this area to fully elucidate causal or correlational relationships.

MAP3K5 Protein's Applications

Applications of MAP3K5 protein lie predominantly within the research and medicinal fields. As it plays a pivotal role in diseases like Parkinson's, Alzheimer's, and certain cancers, it is the subject of rigorous studies aiming to establish new treatment modalities. The protein's role in critical pathways and processes has drawn scientific interest, making it a target for drug discovery and development.

Targeting the MAP3K5 protein could potentially mitigate the progression of neurodegenerative diseases and slow cancer growth. Nevertheless, while the promise is evident, further research is required to ensure these treatments' safety and efficacy, considering the MAP3K5 protein's broad impact across various cellular functions.

• ancer research: Map3k5, also known as apoptosis signal-regulating kinase 1 (ASK1), is involved in regulating cell proliferation and survival. Dysregulation of Map3k5 signaling has been implicated in various types of cancers. Targeting Map3k5 signaling pathway may have potential therapeutic implications in cancer treatment.
•  Neurodegenerative diseases: Map3k5 signaling has been linked to neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. Understanding the role of Map3k5 in neuronal cell death and neuroinflammation may help in the development of novel therapeutic strategies for these conditions.
•  Cardiovascular diseases: Map3k5 has been implicated in the development and progression of cardiovascular diseases, including hypertension and atherosclerosis. Modulating Map3k5 signaling pathway may provide new insights into the treatment of these conditions.

MAP3K5 has several biochemical functions, for example, ATP binding,MAP kinase kinase kinase activity,magnesium ion binding. Some of the functions are cooperated with other proteins, some of the functions could acted by MAP3K5 itself. We selected most functions MAP3K5 had, and list some proteins which have the same functions with MAP3K5. You can find most of the proteins on our site.

MAP3K5 has direct interactions with proteins and molecules. Those interactions were detected by several methods such as yeast two hybrid, co-IP, pull-down and so on. We selected proteins and molecules interacted with MAP3K5 here. Most of them are supplied by our site. Hope this information will be useful for your research of MAP3K5.

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