PA5-24634

antibody from Invitrogen Antibodies

Targeting: GOT1 AST1

Provider product page for PA5-24634

Western blot

Immunohistochemistry

Flow cytometry

Other assay

Antibody data

Antibody Data
Antigen structure
References [2]
Comments [0]
Validations
Flow cytometry [1]
Other assay [2]

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Product number: PA5-24634 - Provider product page
Provider: Invitrogen Antibodies
Product name: GOT1 Polyclonal Antibody
Antibody type: Polyclonal
Antigen: Synthetic peptide
Description: This antibody is predicted to react with rat based on sequence homology.
Reactivity: Human
Host: Rabbit
Isotype: IgG
Vial size: 400 µL
Concentration: 0.5 mg/mL
Storage: Store at 4°C short term. For long term storage, store at -20°C, avoiding freeze/thaw cycles.

GOT1 protein structure - PA5-24634 shown in red.

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Fig. 3 Glutaminolysis mediates miR-137-induced ferroptosis inhibition. a Schematic overview of the glutaminolysis pathway in ferroptosis. Glutamine (Gln) is transferred into cell cytoplasm by importers SLC1A5/SLC38A1, and subsequently converted to glutamate (Glu) by glutaminase GLS2 in mitochondria. The aspartate transaminase GOT1 ultimately converts Glu to a-ketoglutarate (a-KG), which contributes to ROS accumulation by an unknown mechanism. The small-molecule inhibitors are indicated in red: L-Gln transporter inhibitor GPNA; GLS inhibitor Compound 968; Pan-transaminases inhibitor AOA. b Pharmacological inhibition of multiple components in the glutaminolysis pathway abrogated anti-miR-137-mediated ferroptosis cell death and lipid accumulation. Cells transfected with control or miR-137 antagomirs were treated with erastin (5 uM) and GPNA (5 mM)/compound 968 (20 uM)/AOA (0.5 mM) for 24 h. The cell viability was assayed using a CCK-8 kit and the lipid accumulation was measured by MDA assay. Data shown represent mean +- SD from three independent experiments. n.s. nonsignificant; ** p < 0.01. c Knockdown of Gln importers or metabolic enzymes blocked anti-miR-137-mediated ferroptosis cell death and lipid accumulation. Cells stably expressing control shRNA or indicated shRNA targeting metabolic enzymes were transfected with control or miR-137 antagomir, and then treated with erastin (5 uM) for 24 h. The cell viability was assayed using a CCK-8 kit and the lipid accumulation was mea

Supportive validation

Submitted by: Invitrogen Antibodies (provider)
Main image
Experimental details: Fig. 1 Continuous low-dose cisplatin pressure changed the expression patterns of hsa_circRNA_103809, miR-377-3p and GOT1 in NSCLC cells. The parental CS-NSCLC cells (A549, H1299 and Calu-3) were subjected to continuous low-dose cisplatin treatment to generate CR-NSCLC cells (A549/DDP, H1299/DDP and Calu-3/DDP). a-c Cell proliferation abilities in CS-NSCLC and CR-NSCLC cells were determined by using the CCK-8 assay (Note: ""Control: without cisplatin stimulation""). d-f Trypan blue staining assay was conducted to evaluate NSCLC cell viability. g Cell apoptosis ratio was measured by using the Annexin V-FITC/PI double staining method. Real-Time qPCR was used to examine the expression levels of ( h ) hsa_circRNA_103809, i miR-377-3p and j GOT1 mRNA in NSCLC cells. k Western Blot analysis was employed to determine the protein levels of GOT1 in NSCLC cells, full-length blots/gels are presented in Supplementary Figure S 4 . Each experiment was repeated at least 3 times. * P < 0.05