Denticleless Protein Homolog (DTL) Antibody

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Description
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 and CDKN1A/p21 (CIP1). CDT1 degradation in response to DNA damage is necessary to ensure proper cell cycle regulation of DNA replication. CDKN1A/p21 (CIP1) degradation during S phase or following UV irradiation is essential to control replication licensing. 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.
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Product specifications
Category | Primary Antibodies |
Immunogen Target | Denticleless Protein Homolog (DTL) |
Host | Rabbit |
Reactivity | Human, Mouse |
Recommended Dilution | WB: 1/1000, FCM: 1/10 - 1/50. Optimal dilutions/concentrations should be determined by the end user. |
Clonality | Polyclonal |
Conjugation | Unconjugated |
Isotype | IgG |
Purification | Purified through a protein A column, followed by peptide affinity purification. |
Size 1 | 80 µl |
Size 2 | 400 µl |
Form | Liquid |
Tested Applications | ELISA, WB, FCM |
Buffer | PBS containing 0.09% sodium azide. |
Availability | Shipped within 5-10 working days. |
Storage | Aliquot and store at -20°C. Avoid repeated freeze/thaw cycles. |
Dry Ice | No |
UniProt ID | Q9NZJ0 |
Background | Antibody anti-DTL |
Status | RUO |
Descripción
Related Products

DTL antibody
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), FBXO18/FBH1 and KMT5A(PubMed:16861906, PubMed:16949367, PubMed:16964240, PubMed:17085480, PubMed:18703516, PubMed:18794347, PubMed:18794348, PubMed:19332548, PubMed:20129063, PubMed:23478441, PubMed:23478445, PubMed:23677613). 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).
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DTL antibody
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), FBXO18/FBH1 and KMT5A(PubMed:16861906, PubMed:16949367, PubMed:16964240, PubMed:17085480, PubMed:18703516, PubMed:18794347, PubMed:18794348, PubMed:19332548, PubMed:20129063, PubMed:23478441, PubMed:23478445, PubMed:23677613). 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).
Ver Producto
Denticleless Protein Homolog (DTL) Antibody
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 and CDKN1A/p21 (CIP1). CDT1 degradation in response to DNA damage is necessary to ensure proper cell cycle regulation of DNA replication. CDKN1A/p21 (CIP1) degradation during S phase or following UV irradiation is essential to control replication licensing. 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.
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