FTO Antibody

Our mouse monoclonal FTO total protein antibody is Protein G purified. It is excellent for use in WB and ICC.

Catalog #: 597-FTO Categories: , Datasheet:

$119.00$380.00

  • SizePrice
Clear
Formulation:
Protein G Purified
Species Tested:
Human, Mouse, Rat
Expected Reactivity:
Bovine, Canine, Non-human primate, sheep
Applications:
WB 1:1000ICC 1:100-1:600 Don't see your application?
Host Species:
Mouse Monoclonal
Gene Name:
FTO
Molecular Weight:
~58 kDa
Cite This Antibody:
PhosphoSolutions Cat# 597-FTO, RRID:AB_2492098
Antigen/Purification: ExpandCollapse

The antigen is synthetic peptide from the N-terminal region of rat FTO.

The antibody is Protein G purified culture supernatant.

Biological Significance: ExpandCollapse

The FTO gene is the most robust gene for common obesity characterized to date. FTO gene expression has been found to be significantly upregulated in the hypothalamus of rats after food deprivation and strongly negatively correlated with the expression of orexin peptide which is involved in the stimulation of food intake (Fredricksson R et al., 2008). Deletion analysis of FTO gene in mice showed that FTO is functionally involved in the control of both energy intake and energy expenditure (Fischer J et al., 2009).

Synonyms: ExpandCollapse

• AlkB homolog 9 antibody
• ALKBH9 antibody
• Alpha-ketoglutarate-dependent dioxygenase FTO antibody
• AW743446 antibody
• Fat mass and obesity-associated protein antibody
• FATSO, MOUSE, HOMOLOG OF antibody
• Fto antibody
• FTO_HUMAN antibody
• GDFD antibody
• KIAA1752 antibody
• mKIAA1752 antibody
• Protein fatso antibody

Storage

100 µl in 10 mM HEPES (pH 7.5), 150 mM NaCl, 100 µg BSA per ml and 50% glycerol. Adequate amount of material to conduct 10-mini Western Blots.

For long term storage –20° C is recommended in undiluted aliquots. Stable at –20° C for up to one year after date of receipt. Avoid freeze/thaw cycles.

Product Specific Protocols

Immunocytochemistry

Mouse Embryonic Fibroblasts (MEFs)

Western Blotting

Click here to view our protocols page for Western blotting and lysate preparation.

Product Specific References for Applications and Species

Immunohistochemistry: Human | Mouse | Rat

Western Blot: Human | Mouse | Rat


Immunohistochemistry: Human
PMIDDilutionPublication
21963515not listedHoorn, E.J., et al. 2011. The calcineurin inhibitor tacrolimus activates the renal sodium chloride cotransporter to cause hypertension. Nature medicine, 17(10), p.1304.


Immunohistochemistry: Mouse
PMIDDilutionPublication
305178561:100Saritas, T., et al. 2018. Optical Clearing in the Kidney Reveals Potassium-Mediated Tubule Remodeling. Cell reports, 25(10), pp.2668-2675.
294127041:10,000Terker, A.S., et al. 2018. With no lysine kinase 4 modulates sodium potassium 2 chloride cotransporter activity in vivo. American Journal of Physiology-Renal Physiology, 315(4), pp.F781-F790.
292632981:10,000Ferdaus, M.Z., et al. 2017. Mutant Cullin 3 causes familial hyperkalemic hypertension via dominant effects. JCI insight, 2(24).
24799612not listedTerker, A.S., et al. 2014. Sympathetic stimulation of thiazide-sensitive sodium chloride cotransport in the generation of salt-sensitive hypertension. Hypertension, 64(1), pp.178-184.
22651238not listedKomers, R., et al. 2012. Enhanced phosphorylation of Na+–Cl− co-transporter in experimental metabolic syndrome: role of insulin. Clinical science, 123(11), pp.635-647.
21963515not listedHoorn, E.J., et al. 2011. The calcineurin inhibitor tacrolimus activates the renal sodium chloride cotransporter to cause hypertension. Nature medicine, 17(10), p.1304.
219071411:500McCormick, J.A., et al. 2011. A SPAK isoform switch modulates renal salt transport and blood pressure. Cell metabolism, 14(3), pp.352-364.
21896937not listedMcCormick, J.A., et al. 2011. Overexpression of the sodium chloride cotransporter is not sufficient to cause familial hyperkalemic hypertension. Hypertension, 58(5), 888-894.


Immunohistochemistry: Rat
PMIDDilutionPublication
22651238not listedKomers, R., et al. 2012. Enhanced phosphorylation of Na+–Cl− co-transporter in experimental metabolic syndrome: role of insulin. Clinical science, 123(11), pp.635-647.
21896937not listedMcCormick, J.A., et al. 2011. Overexpression of the sodium chloride cotransporter is not sufficient to cause familial hyperkalemic hypertension. Hypertension, 58(5), 888-894.


Western Blot: Human
PMIDDilutionPublication
295477031:2000Tutakhel, O.A., et al. 2018. Dominant functional role of the novel phosphorylation site S811 in the human renal NaCl cotransporter. The FASEB Journal, pp.fj-201701047R.
21963515not listedHoorn, E.J., et al. 2011. The calcineurin inhibitor tacrolimus activates the renal sodium chloride cotransporter to cause hypertension. Nature medicine, 17(10), p.1304.


Western Blot: Mouse
PMIDDilutionPublication
317678461:1000Mao, Y., et al. 2019. . m 6 A in mRNA coding regions promotes translation via the RNA helicase-containing YTHDC2. Nature communications, 10(1), pp.1-11.
31239388not listedWu, P., et al. 2019. . Deletion of Kir5. 1 Impairs Renal Ability to Excrete Potassium during Increased Dietary Potassium Intake. Journal of the American Society of Nephrology, Aug;30(8):1425-1438.
30728179not listedKhamaysi, A., et al. 2019. Systemic Succinate Homeostasis and Local Succinate Signaling Affect Blood Pressure and Modify Risks for Calcium Oxalate Lithogenesis. Journal of the American Society of Nephrology, pp.ASN-2018030277.
305715581:1000Duan, X.P., et al. 2019. Norepinephrine-Induced Stimulation of Kir4. 1/Kir5. 1 Is Required for the Activation of NaCl Transporter in Distal Convoluted Tubule. Hypertension,73:112-120.
30355950not listedXu, J., et al. 2018. Slc4a8 in the Kidney: Expression, Subcellular Localization and Role in Salt Reabsorption. Cellular Physiology and Biochemistry, 50(4), pp.1361-1375.
303018601:2000Cornelius, R.J., et al. 2018. Renal COP9 signalosome deficiency alters CUL3-KLHL3-WNK signaling pathway. Journal of the American Society of Nephrology, 29(11), pp.2627-2640.
302525331:1000Cherezova, A., et al. 2018. Urinary concentrating defect in mice lacking Epac1 or Epac2. The FASEB Journal, pp.fj-201800435R.
294127041:2000Terker, A.S., et al. 2018. With no lysine kinase 4 modulates sodium potassium 2 chloride cotransporter activity in vivo. American Journal of Physiology-Renal Physiology, 315(4), pp.F781-F790.
293108251:6000Wang, M.X., et al. 2018. Potassium intake modulates the thiazide-sensitive sodium-chloride cotransporter (NCC) activity via the Kir4. 1 potassium channel. Kidney international, 93(4), pp.893-902.
292632981:2000Ferdaus, M.Z., et al. 2017. Mutant Cullin 3 causes familial hyperkalemic hypertension via dominant effects. JCI insight, 2(24).
280529881:1000Cuevas, C.A., et al. 2017. Potassium sensing by renal distal tubules requires Kir4. 1. Journal of the American Society of Nephrology, 28(6), pp.1814-1825.
270684411:2000Ferdaus, M.Z., et al. 2016. SPAK and OSR1 play essential roles in potassium homeostasis through actions on the distal convoluted tubule. The Journal of physiology, 594(17), pp.4945-4966.
26712527not listedTerker, A.S., et al. 2016. Direct and Indirect Mineralocorticoid Effects Determine Distal Salt Transport. J Am Soc Nephrol. (8):2436-45
264329041:6000Lazelle, R.A., et al. 2016. Renal deletion of 12 kDa FK506-binding protein attenuates tacrolimus-induced hypertension. Journal of the American Society of Nephrology, 27(5), pp.1456-1464.
26422504not listedTerker, A.S., et al. 2015. Unique chloride-sensing properties of WNK4 permit the distal nephron to modulate potassium homeostasis. Kidney international, 89(1), pp.127-134.
25565204not listedTerker, A.S., et al. 2015. Potassium modulates electrolyte balance and blood pressure through effects on distal cell voltage and chloride. Cell Metab. (1):39-50.
25250572not listedMcCormick, J.A., et al. 2014. Hyperkalemic hypertension–associated cullin 3 promotes WNK signaling by degrading KLHL3. The Journal of clinical investigation, 124(11), pp.4723-4736.
25113964not listed Chávez -Canales, M., et al. 2014. WNK-SPAK-NCC cascade revisited: WNK1 stimulates the activity of the Na-Cl cotransporter via SPAK, an effect antagonized by WNK4. Hypertension, 64(5), pp.1047-1053.
24799612not listedTerker, A.S., et al. 2014. Sympathetic stimulation of thiazide-sensitive sodium chloride cotransport in the generation of salt-sensitive hypertension. Hypertension, 64(1), pp.178-184.
242316591:5000Picard, N., et al. 2014. . Protein phosphatase 1 inhibitor-1 deficiency reduces phosphorylation of renal NaCl cotransporter and causes arterial hypotension. Journal of the American Society of Nephrology, 25(3), pp.511-522.
22651238not listedKomers, R., et al. 2012. Enhanced phosphorylation of Na+–Cl− co-transporter in experimental metabolic syndrome: role of insulin. Clinical science, 123(11), pp.635-647.
21963515not listedHoorn, E.J., et al. 2011. The calcineurin inhibitor tacrolimus activates the renal sodium chloride cotransporter to cause hypertension. Nature medicine, 17(10), p.1304.
21907141not listedMcCormick, J.A., et al. 2011. A SPAK isoform switch modulates renal salt transport and blood pressure. Cell metabolism, 14(3), pp.352-364.
21896937not listedMcCormick, J.A., et al. 2011. Overexpression of the sodium chloride cotransporter is not sufficient to cause familial hyperkalemic hypertension. Hypertension, 58(5), 888-894.


Western Blot: Rat
PMIDDilutionPublication
28931751not listedPalygin, O., et al. 2017. Essential role of K ir 5.1 channels in renal salt handling and blood pressure control. JCI Insight, 2(18).
22651238not listedKomers, R., et al. 2012. Enhanced phosphorylation of Na+–Cl− co-transporter in experimental metabolic syndrome: role of insulin. Clinical science, 123(11), pp.635-647.
21896937not listedMcCormick, J.A., et al. 2011. Overexpression of the sodium chloride cotransporter is not sufficient to cause familial hyperkalemic hypertension. Hypertension, 58(5), 888-894.

  • 5 – Excellent (publishable, performed ideally)
  • 4 – Good (publishable, would use again)
  • 3 – Average (publishable, might use again)
  • 2 – Poor (unpublishable, signal inconclusive)
  • 1 – No signal (unpublishable)
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