CYLN2 Antibody | 59-428

CYLN2 Antibody | 59-428 | Gentaur UK, US & Europe Distribution

Host: Rabbit

Reactivity: Human, Mouse

Homology: Predicted species reactivity based on immunogen sequence: Rat

Immunogen: This CYLN2 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 911-940 amino acids from the C-terminal region of human CYLN2.

Research Area: Neuroscience, Signal Transduction

Tested Application: WB

Application: For WB starting dilution is: 1:1000

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: 116 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: CAP-Gly domain-containing linker protein 2, Cytoplasmic linker protein 115, CLIP-115, Cytoplasmic linker protein 2, Williams-Beuren syndrome chromosomal region 3 protein, Williams-Beuren syndrome chromosomal region 4 protein, CLIP2, CYLN2, KIAA0291, WBSCR3, WBSCR4, WSCR4

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

BACKGROUND: The protein encoded by this gene belongs to the family of cytoplasmic linker proteins, which have been proposed to mediate the interaction between specific membranous organelles and microtubules. This protein was found to associate with both microtubules and an organelle called the dendritic lamellar body. This gene is hemizygously deleted in Williams syndrome, a multisystem developmental disorder caused by the deletion of contiguous genes at 7q11.23. Alternative splicing of this gene generates 2 transcript variants.