MLXIPL Antibody | 56-508

MLXIPL Antibody | 56-508 | Gentaur UK, US & Europe Distribution

Host: Rabbit

Reactivity: Human, Mouse

Homology: N/A

Immunogen: This MLXIPL antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 624-653 amino acids from the C-terminal region of human MLXIPL.

Research Area: Cancer, Obesity

Tested Application: WB, IHC-P

Application: For WB starting dilution is: 1:2000
For IHC-P 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: 93 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: Carbohydrate-responsive element-binding protein, ChREBP, Class D basic helix-loop-helix protein 14, bHLHd14, MLX interactor, MLX-interacting protein-like, WS basic-helix-loop-helix leucine zipper protein, WS-bHLH, Williams-Beuren syndrome chromosomal region 14 protein, MLXIPL, BHLHD14, MIO, WBSCR14

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

BACKGROUND: This gene encodes a basic helix-loop-helix leucine zipper transcription factor of the Myc/Max/Mad superfamily. This protein forms a heterodimeric complex and binds and activates, in a glucose-dependent manner, carbohydrate response element (ChoRE) motifs in the promoters of triglyceride synthesis genes. The gene is deleted in Williams-Beuren syndrome, a multisystem developmental disorder caused by the deletion of contiguous genes at chromosome 7q11.23.