GOLPH3 Antibody | 5443

GOLPH3 Antibody | 5443 | Gentaur UK, US & Europe Distribution

Host: Rabbit

Reactivity: Human, Mouse, Rat

Homology: N/A

Immunogen: GOLPH3 antibody was raised against a 14 amino acid synthetic peptide from near the amino terminus of human GOLPH3.
The immunogen is located within the first 50 amino acids of GOLPH3.

Research Area: Cancer

Tested Application: E, WB, IF

Application: GOLPH3 antibody can be used for detection of GOLPH3 by Western blot at 0.5 - 1 μg/mL. For immunofluorescence start at 20 μg/mL.
Antibody validated: Western Blot in rat samples and Immunofluorescence in rat samples. All other applications and species not yet tested.

Specificiy: N/A

Positive Control 1: Cat. No. 1462 - Rat Lung Tissue Lysate

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: N/A

Validation: N/A

Isoform: N/A

Purification: GOLPH3 Antibody is affinity chromatography purified via peptide column.

Clonality: Polyclonal

Clone: N/A

Isotype: IgG

Conjugate: Unconjugated

Physical State: Liquid

Buffer: GOLPH3 Antibody is supplied in PBS containing 0.02% sodium azide.

Concentration: 1 mg/mL

Storage Condition: GOLPH3 antibody can be stored 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: GOLPH3 Antibody: GOPP1, GPP34, MIDAS, Golgi phosphoprotein 3, Coat protein GPP34

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

BACKGROUND: GOLPH3 Antibody: GOLPH3 was initially identified as a peripheral membrane protein localized to the trans-Golgi network, but others reported it to be primarily a mitochondrial protein that regulated the mitochondrial mass through the regulation of the mitochondria-specific phospholipid cardiolipin. GOLPH3 has since been implicated in the target of rapamycin (TOR) signalling pathway. Its overexpression in transfected cells led to and increase in anchorage-independent growth and cell proliferation in vitro. Furthermore, GOLPH3-transfected cells enhanced S6 Kinase activity in response to growth factor stimulation by EGF. Simultaneously, AKT phosphorylation increased in these cells, while these events were abrogated in GOLPH3 siRNA treated cells compared to control cells, indicating the GOLPH3 can enhance signalling through TOR-associated complexes. These results suggest that GOLPH3 is a bona fide oncogene and may be a useful target for therapeutic strategies.