NIP1 Antibody | 56-890

NIP1 Antibody | 56-890 | Gentaur UK, US & Europe Distribution

Host: Rabbit

Reactivity: Human, Mouse

Homology: N/A

Immunogen: This NIP1 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 92-127 amino acids from human NIP1.

Research Area: Cell Cycle, Neuroscience, Signal Transduction

Tested Application: WB, IHC-P

Application: For WB starting dilution is: 1:1000
For IHC-P starting dilution is: 1:50~100

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: 26 kDa

Validation: N/A

Isoform: N/A

Purification: This antibody is prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by dialysis

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: Vesicle transport protein SEC20, BCL2/adenovirus E1B 19 kDa protein-interacting protein 1, Transformation-related gene 8 protein, TRG-8, BNIP1, NIP1, SEC20L

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

BACKGROUND: NIP1 (BNIP1) is a member of the BCL2/adenovirus E1B 19 kd-interacting protein (BNIP) family. It interacts with the E1B 19 kDa protein which is responsible for the protection of virally-induced cell death, as well as E1B 19 kDa-like sequences of BCL2, also an apoptotic protector. Alternative splicing of this gene results in four products of unknown function. Transcript variant BNIP1 contains the entire coding region of the gene. This variant contains a fully conserved BH3 domain, which has been associated with pro-apoptotic function.