DTL Antibody | 55-536

DTL Antibody | 55-536 | Gentaur UK, US & Europe Distribution

Host: Rabbit

Reactivity: Human, Mouse

Homology: N/A

Immunogen: This DTL antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 229-256 amino acids from the Central region of human DTL.

Research Area: Cell Cycle

Tested Application: WB, Flow

Application: For WB starting dilution is: 1:1000
For FACS starting dilution is: 1:10~50

Specificiy: N/A

Positive Control 1: N/A

Positive Control 2: N/A

Positive Control 3: N/A

Positive Control 4: N/A

Positive Control 5: N/A

Positive Control 6: N/A

Molecular Weight: 79 kDa

Validation: N/A

Isoform: N/A

Purification: This antibody is purified through a protein A column, followed by peptide affinity purification.

Clonality: Polyclonal

Clone: N/A

Isotype: Rabbit Ig

Conjugate: Unconjugated

Physical State: Liquid

Buffer: Supplied in PBS with 0.09% (W/V) sodium azide.

Concentration: batch dependent

Storage Condition: Store at 4˚C for three months and -20˚C, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.

Alternate Name: Denticleless protein homolog, DDB1- and CUL4-associated factor 2, Lethal (2) denticleless protein homolog, Retinoic acid-regulated nuclear matrix-associated protein, DTL, CDT2, CDW1, DCAF2, L2DTL, RAMP

User Note: Optimal dilutions for each application to be determined by the researcher.

BACKGROUND: 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.