DHCR7 Antibody | 55-855

DHCR7 Antibody | 55-855 | Gentaur UK, US & Europe Distribution

Host: Rabbit

Reactivity: Human, Mouse

Homology: N/A

Immunogen: This DHCR7 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 437-463 amino acids from the C-terminal region of human DHCR7.

Research Area: Cancer, Obesity, Signal Transduction

Tested Application: WB, IHC-P, IF

Application: For IF starting dilution is: 1:25
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: 54 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: 7-dehydrocholesterol reductase, 7-DHC reductase, Putative sterol reductase SR-2, Sterol Delta (7) -reductase, DHCR7, D7SR

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

BACKGROUND: This gene encodes an enzyme that removes the C (7-8) double bond in the B ring of sterols and catalyzes the conversion of 7-dehydrocholesterol to cholesterol. This gene is ubiquitously expressed and its transmembrane protein localizes to the endoplasmic reticulum membrane and nuclear outer membrane. Mutations in this gene cause Smith-Lemli-Opitz syndrome (SLOS) ; a syndrome that is metabolically characterized by reduced serum cholesterol levels and elevated serum 7-dehydrocholesterol levels and phenotypically characterized by mental retardation, facial dysmorphism, syndactyly of second and third toes, and holoprosencephaly in severe cases to minimal physical abnormalities and near-normal intelligence in mild cases. Alternative splicing results in multiple transcript variants that encode the same protein.