DTL: A Potential Cancer and Biomarker Treatment (G51514)
DTL: A Potential Cancer and Biomarker Treatment
DTL (Dihydrothene) is a drug candidate for the treatment of various diseases, including cancer. It works by inhibiting the enzyme dihydrothene reductase (DHR), which is involved in the production of dihydrothene, a key precursor of and family, including testosterone and estradiol.
Dihydrothene is a potent inhibitor of DHR, and has been shown to be effective in preclinical studies against a variety of cancer types, including breast, ovarian, and prostate cancers. It works by binding to the enzyme and inhibiting its activity, which results in a decrease in the production of dihydrothene.
In addition to its potential use as a cancer treatment, DTL has also been shown to be a potential biomarker for the disease. By measuring the levels of dihydrothene in the body, researchers can monitor the effectiveness of a treatment and determine if it is having the desired effect.
DTL has also been shown to be effective in treating other conditions, including inflammation and fibrosis. In these cases, it works by inhibiting the production of dihydrothene and causing a decrease in the production of other unwanted substances in the body.
TheDTL variant 1 is an advanced form of the drug candidate, it is a small molecule inhibitor of DHR with higher affinity for DHR thanDTL variant 2.
DTL has been shown to be effective in preclinical studies against various types of cancer, including breast, ovarian, and prostate cancers. It works by binding to the enzyme and inhibiting its activity, which results in a decrease in the production of dihydrothene.
In addition to its potential use as a cancer treatment, DTL has also been shown to be a potential biomarker for the disease. By measuring the levels of dihydrothene in the body, researchers can monitor the effectiveness of a treatment and determine if it is having the desired effect.
DTL has also been shown to be effective in treating other conditions, including inflammation and fibrosis. In these cases, it works by inhibiting the production of dihydrothene and causing a decrease in the production of other unwanted substances in the body.
TheDTL variant 1 is an advanced form of the drug candidate, it is a small molecule inhibitor of DHR with higher affinity for DHR thanDTL variant 2. It has been shown to be more potent than previous versions and has a more narrow range of inhibition.
DTL has been shown to be effective in preclinical studies against various types of cancer, including breast, ovarian, and prostate cancers. It works by binding to the enzyme and inhibiting its activity, which results in a decrease in the production of dihydrothene.
In addition to its potential use as a cancer treatment, DTL has also been shown to be a potential biomarker for the disease. By measuring the levels of dihydrothene in the body, researchers can monitor the effectiveness of a treatment and determine if it is having the desired effect.
DTL has also been shown to be effective in treating other conditions, including inflammation and fibrosis. In these cases, it works by inhibiting the production of dihydrothene and causing a decrease in the production of other unwanted substances in the body.
TheDTL variant 1 is an advanced form of the drug candidate, it is a small molecule inhibitor of DHR with higher affinity for DHR thanDTL variant 2. It has been shown to be more potent than previous versions and has a more narrow range of inhibition.
In conclusion, DTL (Dihydrothene) is a drug candidate that has the potential to be a valuable cancer and biomarker treatment. Its ability to inhibit the production of dihydrothene, a key precursor of dihydrothene, including testosterone and estradiol, makes it an attractive option for the treatment of various diseases. Additionally, its potential use as a biomarker for monitoring the effectiveness of a treatment makes it an important tool for researchers to study the disease.
Protein Name: Denticleless E3 Ubiquitin Protein Ligase Homolog
Functions: Substrate-specific adapter of a DCX (DDB1-CUL4-X-box) E3 ubiquitin-protein ligase complex required for cell cycle control, DNA damage response and translesion DNA synthesis. The DCX(DTL) complex, also named CRL4(CDT2) complex, mediates the polyubiquitination and subsequent degradation of CDT1, CDKN1A/p21(CIP1), FBH1, KMT5A and SDE2 (PubMed:16861906, PubMed:16949367, PubMed:16964240, PubMed:17085480, PubMed:18703516, PubMed:18794347, PubMed:18794348, PubMed:19332548, PubMed:20129063, PubMed:23478441, PubMed:23478445, PubMed:23677613, PubMed:27906959). CDT1 degradation in response to DNA damage is necessary to ensure proper cell cycle regulation of DNA replication (PubMed:16861906, PubMed:16949367, PubMed:17085480). CDKN1A/p21(CIP1) degradation during S phase or following UV irradiation is essential to control replication licensing (PubMed:18794348, PubMed:19332548). KMT5A degradation is also important for a proper regulation of mechanisms such as TGF-beta signaling, cell cycle progression, DNA repair and cell migration (PubMed:23478445). Most substrates require their interaction with PCNA for their polyubiquitination: substrates interact with PCNA via their PIP-box, and those containing the 'K+4' motif in the PIP box, recruit the DCX(DTL) complex, leading to their degradation. In undamaged proliferating cells, the DCX(DTL) complex also promotes the 'Lys-164' monoubiquitination of PCNA, thereby being involved in PCNA-dependent translesion DNA synthesis (PubMed:20129063, PubMed:23478441, PubMed:23478445, PubMed:23677613). The DDB1-CUL4A-DTL E3 ligase complex regulates the circadian clock function by mediating the ubiquitination and degradation of CRY1 (PubMed:26431207)
More Common Targets
DTNA | DTNB | DTNB-AS1 | DTNBP1 | DTWD1 | DTWD2 | DTX1 | DTX2 | DTX2P1 | DTX2P1-UPK3BP1-PMS2P11 | DTX3 | DTX3L | DTX4 | DTYMK | Dual Specificity Mitogen-Activated Protein Kinase Kinase (MEK) | Dual specificity protein kinase (CLK) | Dual specificity protein tyrosine phosphatase | Dual-Specificity Tyrosine-(Y)-Phosphorylation Regulated Kinase 1 | DUBR | DUOX1 | DUOX2 | DUOXA1 | DUOXA2 | DUS1L | DUS2 | DUS3L | DUS4L | DUSP1 | DUSP10 | DUSP11 | DUSP12 | DUSP13 | DUSP14 | DUSP15 | DUSP16 | DUSP18 | DUSP19 | DUSP2 | DUSP21 | DUSP22 | DUSP23 | DUSP26 | DUSP28 | DUSP29 | DUSP3 | DUSP4 | DUSP5 | DUSP5P1 | DUSP6 | DUSP7 | DUSP8 | DUSP8P5 | DUSP9 | DUT | DUTP6 | DUX1 | DUX3 | DUX4 | DUX4L1 | DUX4L13 | DUX4L16 | DUX4L18 | DUX4L19 | DUX4L2 | DUX4L20 | DUX4L23 | DUX4L3 | DUX4L37 | DUX4L4 | DUX4L5 | DUX4L6 | DUX4L7 | DUX4L8 | DUX4L9 | DUXA | DUXAP10 | DUXAP3 | DUXAP8 | DUXAP9 | DVL1 | DVL2 | DVL3 | DXO | DYDC1 | DYDC2 | DYM | Dynactin | DYNAP | DYNC1H1 | DYNC1I1 | DYNC1I2 | DYNC1LI1 | DYNC1LI2 | DYNC2H1 | DYNC2I1 | DYNC2I2 | DYNC2LI1 | DYNLL1 | DYNLL2 | DYNLRB1