Antibody data
- Antibody Data
- Antigen structure
- References [1]
- Comments [0]
- Validations
- Western blot [1]
- Other assay [1]
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Validation data
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- Product number
- PA5-64610 - Provider product page
- Provider
- Invitrogen Antibodies
- Product name
- Phospho-SIK1 (Thr182) Polyclonal Antibody
- Antibody type
- Polyclonal
- Antigen
- Synthetic peptide
- Description
- Phospho-SIK1 (Thr182) Polyclonal Antibody detects endogenous levels of SIK1 only when phosphorylated at Thr182.
- Reactivity
- Human, Rat
- Host
- Rabbit
- Isotype
- IgG
- Vial size
- 100 µL
- Concentration
- 1 mg/mL
- Storage
- -20°C
Submitted references Activation of SIK1 by phanginin A inhibits hepatic gluconeogenesis by increasing PDE4 activity and suppressing the cAMP signaling pathway.
Liu S, Huang S, Wu X, Feng Y, Shen Y, Zhao QS, Leng Y
Molecular metabolism 2020 Nov;41:101045
Molecular metabolism 2020 Nov;41:101045
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Supportive validation
- Submitted by
- Invitrogen Antibodies (provider)
- Main image
- Experimental details
- Western blot analysis of SIK1 in EGF treated HeLa whole cell lysates using a Phospho-SIK1 (Thr182) Polyclonal Antibody (Product # PA5-64610).
Supportive validation
- Submitted by
- Invitrogen Antibodies (provider)
- Main image
- Experimental details
- Chronic treatment of phanginin A improved metabolic disorders in ob/ob mice. Male ob/ob mice were treated with phanginin A (100 mg/kg, once daily, p. o. ), metformin (250 mg/kg, once daily, p. o. ), or vehicle for 26 days. (A-B) Random (A) and fasting blood glucose levels (B) were detected on days 4, 8, 12, 16, 20, 23, and 26. (C) Oral glucose tolerance tests were conducted on day 23. (D) HbA1c was determined on day 26. (E-F) Food intake accumulation (E) and body weight (F) were regularly measured during treatment. (G-H) Triglyceride and total cholesterol in the serum (G) and liver (H) were detected. (I) SIK1 phosphorylation in the liver was analyzed by Western blotting and quantified as the relative optical density. (J) Hepatic PDE4 activity and (K) cAMP concentration were examined after treatment. (L) CREB phosphorylation in the liver was analyzed by Western blotting. (M) Hepatic gluconeogenesis gene expression in ob/ob mice were evaluated. All of the results are presented as the mean +- SEM (n = 8). * P < 0.05 and * * P < 0.01 vs the vehicle group. Figure 8