Unlocking the Potential of ATF4 as a Drug Target and Biomarker

Target Name: ATF4

NCBI ID: G468

ATF4

Unlocking the Potential of ATF4 as a Drug Target and Biomarker

ATF4, or cAMP response element-binding protein 2, is a protein that plays a crucial role in various cellular processes, including cell signaling, DNA replication, and virus replication. Its function is highly conserved across various species, and it has been implicated in numerous diseases, including cancer, neurodegenerative diseases, and autoimmune disorders. As a result, ATF4 has become an attractive drug target and a potential biomarker for various diseases.

Disease-Related Functions of ATF4

ATF4 has been involved in numerous biological processes that are essential for human health and disease. In cancer, it has been shown to contribute to the development and progression of various types of cancer, including breast, ovarian, and prostate cancers. For instance, ATF4 has been shown to promote the growth and survival of cancer cells, and it has been identified as a potential therapeutic target in these diseases.

In neurodegenerative diseases, such as Alzheimer's and Parkinson's diseases, ATF4 has been implicated in the development and progression of these conditions. Studies have shown that ATF4 levels are affected in these conditions, and that it plays a role in the pathogenesis of these diseases. Additionally, ATF4 has been implicated in the development of various neurotoxins, which are known to contribute to neurodegeneration.

In autoimmune disorders, ATF4 has been shown to play a role in the development and progression of these conditions. For instance, ATF4 has been shown to contribute to the development of rheumatoid arthritis (RA) and other autoimmune diseases.

Potential Therapeutic Strategies

Given the involvement of ATF4 in various diseases, it is an attractive drug target and a potential biomarker. Several potential therapeutic strategies have been proposed to target ATF4 and its functions.

1. inhibition of ATF4 signaling pathways:

Several studies have shown that inhibition of ATF4 signaling pathways can be a potential therapeutic strategy for various diseases, including cancer, neurodegenerative diseases, and autoimmune disorders. For instance, several inhibitors of the cAMP-dependent protein kinase (PKA) have been shown to be effective in inhibiting ATF4 signaling. These inhibitors have been shown to reduce the growth and survival of cancer cells, and they have been identified as potential therapeutic targets for cancer.

1. Activation of ATF4 signaling pathways:

Activation of ATF4 signaling pathways can also be a potential therapeutic strategy for various diseases. For instance, several studies have shown that activation of the cAMP-dependent protein kinase (PKA) signaling pathway can contribute to the development and progression of cancer. Activation of this pathway can also be a potential therapeutic strategy for neurodegenerative diseases and autoimmune disorders.

1. Antibodies against ATF4:

Antibodies against ATF4 have been shown to be effective in targeting and neutralizing ATF4 in various diseases. These antibodies have been shown to reduce the growth and survival of cancer cells, and they have been identified as potential therapeutic targets for cancer.

1. Targeted modulation of ATF4 levels:

Targeted modulation of ATF4 levels can also be a potential therapeutic strategy for various diseases. For instance, studies have shown that modulation of ATF4 levels can be an effective way to treat neurodegenerative diseases, including Alzheimer's and Parkinson's diseases. Additionally, modulation of ATF4 levels has also been shown to be an effective way to treat various autoimmune disorders.

Conclusion

In conclusion, ATF4 is a protein that plays a crucial role in various cellular processes and has been implicated in numerous diseases. Its function is highly conserved across various species, and it has

Protein Name: Activating Transcription Factor 4

Functions: Transcription factor that binds the cAMP response element (CRE) (consensus: 5'-GTGACGT[AC][AG]-3') and displays two biological functions, as regulator of metabolic and redox processes under normal cellular conditions, and as master transcription factor during integrated stress response (ISR) (PubMed:17684156, PubMed:16682973, PubMed:31444471, PubMed:32132707). Binds to asymmetric CRE's as a heterodimer and to palindromic CRE's as a homodimer (By similarity). Core effector of the ISR, which is required for adaptation to various stress such as endoplasmic reticulum (ER) stress, amino acid starvation, mitochondrial stress or oxidative stress (PubMed:32132707). During ISR, ATF4 translation is induced via an alternative ribosome translation re-initiation mechanism in response to EIF2S1/eIF-2-alpha phosphorylation, and stress-induced ATF4 acts as a master transcription factor of stress-responsive genes in order to promote cell recovery (PubMed:32132706, PubMed:32132707). Promotes the transcription of genes linked to amino acid sufficiency and resistance to oxidative stress to protect cells against metabolic consequences of ER oxidation (By similarity). Activates the transcription of NLRP1, possibly in concert with other factors in response to ER stress (PubMed:26086088). Activates the transcription of asparagine synthetase (ASNS) in response to amino acid deprivation or ER stress (PubMed:11960987). However, when associated with DDIT3/CHOP, the transcriptional activation of the ASNS gene is inhibited in response to amino acid deprivation (PubMed:18940792). Together with DDIT3/CHOP, mediates programmed cell death by promoting the expression of genes involved in cellular amino acid metabolic processes, mRNA translation and the terminal unfolded protein response (terminal UPR), a cellular response that elicits programmed cell death when ER stress is prolonged and unresolved (By similarity). Together with DDIT3/CHOP, activates the transcription of the IRS-regulator TRIB3 and promotes ER stress-induced neuronal cell death by regulating the expression of BBC3/PUMA in response to ER stress (PubMed:15775988). May cooperate with the UPR transcriptional regulator QRICH1 to regulate ER protein homeostasis which is critical for cell viability in response to ER stress (PubMed:33384352). In the absence of stress, ATF4 translation is at low levels and it is required for normal metabolic processes such as embryonic lens formation, fetal liver hematopoiesis, bone development and synaptic plasticity (By similarity). Acts as a regulator of osteoblast differentiation in response to phosphorylation by RPS6KA3/RSK2: phosphorylation in osteoblasts enhances transactivation activity and promotes expression of osteoblast-specific genes and post-transcriptionally regulates the synthesis of Type I collagen, the main constituent of the bone matrix (PubMed:15109498). Cooperates with FOXO1 in osteoblasts to regulate glucose homeostasis through suppression of beta-cell production and decrease in insulin production (By similarity). Activates transcription of SIRT4 (By similarity). Regulates the circadian expression of the core clock component PER2 and the serotonin transporter SLC6A4 (By similarity). Binds in a circadian time-dependent manner to the cAMP response elements (CRE) in the SLC6A4 and PER2 promoters and periodically activates the transcription of these genes (By similarity). Mainly acts as a transcriptional activator in cellular stress adaptation, but it can also act as a transcriptional repressor: acts as a regulator of synaptic plasticity by repressing transcription, thereby inhibiting induction and maintenance of long-term memory (By similarity). Regulates synaptic functions via interaction with DISC1 in neurons, which inhibits ATF4 transcription factor activity by disrupting ATF4 dimerization and DNA-binding (PubMed:31444471)

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