TIMELESS: A Non-Coding RNA Molecule Regulating The Circadian Rhythm

Target Name: TIMELESS

NCBI ID: G8914

TIMELESS

TIMELESS: A Non-Coding RNA Molecule Regulating The Circadian Rhythm

The circadian rhythm is a critical internal biological process that regulates various physiological and behavioral processes in living organisms, including humans. The ability of the circadian rhythm to synchronize with the external environment is crucial for maintaining the health and well-being of the organism. Regulation of the circadian rhythm is a complex process that involves multiple mechanisms, including the interaction of light, hormones, and neurotransmitters.

One of the key components of the circadian rhythm is the TIMELESS protein. TIMELESS is a non-coding RNA molecule that plays a critical role in regulating the circadian rhythm in various organisms, including mammals. TIMELESS is composed of 19 different proteins that are arranged in a highly conserved pattern. The protein encoded by TIMELESS contains a unique feature, known as a C-terminal hypervariable region (HVR), which allows for the diversity of the TIMELESS protein family.

TIMELESS function

TIMELESS is involved in the regulation of the circadian rhythm by binding to the clock gene PER2. The clock gene is a key regulator of the circadian rhythm and is responsible for producing the protein PER2, which is a critical component of the circadian clock. TIMELESS binds to the PER2 gene and prevents it from being translated into protein, which inhibits the circadian clock.

In addition to its function in regulating the circadian clock, TIMELESS has also been shown to play a role in various cellular processes that are important for the survival and function of cells. One of the key functions of TIMELESS is its ability to interact with the protein p53, which is a well-known regulator of the DNA damage response. TIMELESS has been shown to play a role in the regulation of p53 activity, which is critical for the DNA damage response and the regulation of cellular processes that are important for the survival and function of cells.

Drug targeting

TIMELESS has been shown to be a potential drug target in the treatment of various diseases. One of the key advantages of targeting TIMELESS is its ability to interact with multiple cellular processes, including the regulation of the circadian clock, the DNA damage response, and cellular signaling pathways. This makes TIMELESS a potentially useful target for the treatment of a wide range of diseases, including sleep disorders, cancer, and neurodegenerative diseases.

Anti-TIMELESS therapy

Anti-TIMELESS therapy is a potential approach to treating various diseases that is based on the inhibition of TIMELESS function. One of the key strategies for anti-TIMELESS therapy is the use of small molecules that can inhibit the activity of TIMELESS and prevent it from binding to the clock gene PER2. One of the potential benefits of anti-TIMELESS therapy is its ability to selectively target TIMELESS and other proteins that are involved in the regulation of the circadian clock, without affecting the activity of other cellular processes.

In addition to its potential benefits, anti-TIMELESS therapy is also a promising approach to treating certain diseases, as it has been shown to have a broad range of potential applications in various fields. For example, anti-TIMELESS therapy has been shown to be effective in the treatment of sleep disorders, including insomnia and sleep apnea. In addition, anti-TIMELESS therapy has also been shown to be effective in the treatment of certain types of cancer, including breast cancer and lung cancer.

Conclusion

TIMELESS is a non-coding RNA molecule that plays a critical role in the regulation of the circadian rhythm. Its function in regulating the circadian rhythm is crucial for the health and well-being of the organism, and its potential as a drug target makes it an attractive target for the treatment of various diseases. The use of small molecules that can inhibit the activity of TIMELESS is a promising approach to anti-TIMELESS therapy, and its potential applications in the treatment of

Protein Name: Timeless Circadian Regulator

Functions: Plays an important role in the control of DNA replication, maintenance of replication fork stability, maintenance of genome stability throughout normal DNA replication, DNA repair and in the regulation of the circadian clock (PubMed:9856465, PubMed:17141802, PubMed:17296725, PubMed:23418588, PubMed:26344098, PubMed:23359676, PubMed:35585232, PubMed:31138685, PubMed:32705708). Required to stabilize replication forks during DNA replication by forming a complex with TIPIN: this complex regulates DNA replication processes under both normal and stress conditions, stabilizes replication forks and influences both CHEK1 phosphorylation and the intra-S phase checkpoint in response to genotoxic stress (PubMed:17141802, PubMed:17296725, PubMed:23359676, PubMed:35585232). During DNA replication, inhibits the CMG complex ATPase activity and activates DNA polymerases catalytic activities, coupling DNA unwinding and DNA synthesis (PubMed:23359676). TIMELESS promotes TIPIN nuclear localization (PubMed:17141802, PubMed:17296725). Plays a role in maintaining processive DNA replication past genomic guanine-rich DNA sequences that form G-quadruplex (G4) structures, possibly together with DDX1 (PubMed:32705708). Involved in cell survival after DNA damage or replication stress by promoting DNA repair (PubMed:17141802, PubMed:17296725, PubMed:26344098, PubMed:30356214). In response to double-strand breaks (DSBs), accumulates at DNA damage sites and promotes homologous recombination repair via its interaction with PARP1 (PubMed:26344098, PubMed:30356214, PubMed:31138685). May be specifically required for the ATR-CHEK1 pathway in the replication checkpoint induced by hydroxyurea or ultraviolet light (PubMed:15798197). Involved in the determination of period length and in the DNA damage-dependent phase advancing of the circadian clock (PubMed:23418588, PubMed:31138685). Negatively regulates CLOCK|NPAS2-ARTNL/BMAL1|ARTNL2/BMAL2-induced transactivation of PER1 possibly via translocation of PER1 into the nucleus (PubMed:9856465, PubMed:31138685). May play a role as destabilizer of the PER2-CRY2 complex (PubMed:31138685). May also play an important role in epithelial cell morphogenesis and formation of branching tubules (By similarity)

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