Salt-Inducible Kinase 2 (SIK2) ELISA Kits

Human Salt-Inducible Kinase 2 (SIK2) interaction partners

1. Data suggest that cAMP/protein kinase A-dependent phosphorylation of SIK1, SIK2, and SIK3 inhibits their catalytic activity by inducing 14-3-3 protein binding.

2. results of this study indicate that SIK2 expression can serve as a prognostic biomarker for EOC and that miR-874-3p and miR-874-5p have the potential to enhance clinical treatment of EOC

3. SIK2 controls osteocyte responses to parathyroid hormone.

4. The results suggest that activation of SIK2 is required for the cell viability when proteasome activity is inhibited by peritoneal dialysis solutions.

5. Data demonstrate that SIK2 and SIK3 mRNA are downregulated in adipose tissue from obese individuals and that the expression is regulated by weight change. SIK2 is also negatively associated with in vivo insulin resistance (HOMA-IR), independently of BMI and age.

6. salt-inducible kinase inhibition decreases proinflammatory cytokines in human myeloid cells upon IL-1R stimulation.

7. Activated SIK2 plays a dual role in augmenting AMPK-induced phosphorylation of acetyl-CoA carboxylase and in activating the PI3K/AKT pathway through p85alpha-S154 phosphorylation. These findings identify SIK2 at the apex of the adipocyte-induced signaling cascades in cancer cells.

8. Findings suggest that SIK2 restricts autophagic flux which in the claudin-low subtype is essential for viability of triple-negative breast cancer cells.

9. Data show that microRNA miR-203 and the salt-inducible kinase 2 (SIK2) are reverse expressed in colorectal tumors.

10. Examination of SIK2 in prostate cancer cells found that it functions both as a positive regulator of cell-cycle progression and a negative regulator of CREB1 activity. Also, the study shows high levels of auto-antibodies against SIK2 in plasma.

11. this study suggests that the tightly linked regulatory loop comprised of the SIK2-PP2A and CaMKI and PME-1 networks may function in fine-tuning cell proliferation and stress response.

12. a mechanism by which the interplay between SIK2 and p97/VCP contributes to the regulation of ERAD in mammalian cells.

13. These findings revealed a new function of LKB1 and salt-inducible kinases as negative regulators of HTLV-1 transcription.

14. tumor suppressor kinase LKB1 activates the downstream kinases SIK2 and SIK3 to stimulate nuclear export of class IIa histone deacetylases

15. findings uncover SIK2 as a critical determinant in autophagy progression and further suggest a mechanism in which the interplay among kinase and deacetylase activities contributes to cellular protein pool homeostasis.

16. In adipocytes, Ser358 (not Ser587) is the main site phosphorylated and responsible for the binding of SIK2 to 14-3-3 proteins.

17. Depletion of SIK2 also delayed G1/S transition and reduced AKT phosphorylation. Higher expression of SIK2 significantly correlated with poor survival in patients with high-grade serous ovarian cancers

18. Increased SIK2 expression is associated with diffuse large B-cell lymphoma.

Mouse (Murine) Salt-Inducible Kinase 2 (SIK2) interaction partners

1. Mutant Gnas is critical for pancreatic tumour tumorigenesis, driven by protein-kinase-A-mediated suppression of salt-inducible kinases (Sik1-3), and associated with induction of lipid remodelling and fatty acid oxidation.

2. SIK2 controls osteocyte responses to parathyroid hormone.

3. SIK-2 participates in inflammation induction after ICH. SIK-2 inhibition via Bosutinib or small interfering RNA decreased inflammation, attenuating brain injury. SIK-2 effects are, at least partly, mediated by CRTC3-cyclic amp-response element binding protein-NF-kappaB signaling pathway.

4. Data, including data from studies conducted with knockout mice, suggest that Pin1 (prolyl isomerase 1) expression in pancreatic beta-cells is markedly elevated in obesity from diet high in fat/sucrose; Pin1 appears to be involved in proliferation of beta-cells and in regulation of secretion of insulin; Pin1 interacts with Sik2 (salt-inducible kinase 2) to regulate calcium signaling.

5. The data highlight an integral role for SIK2 and SIK3 in innate immunity by preventing the differentiation of macrophages into a potent and stable anti-inflammatory phenotype.

6. SIK2 acts directly on CRTC2, CRTC3 and HDAC4, and the cAMP-PKA pathway reduces the interaction of SIK2 with CREB-regulated transcription co-activators and PP2A. Downstream, SIK2 increases GLUT4 levels and glucose uptake in adipocytes.

7. Sik1, Sik2, and Sik3 play a key role as gluconeogenesis suppressors downstream of LKB1 in the liver.

8. study identifies the salt-inducible kinases as major targets of bosutinib and dasatinib that mediate the effects of these drugs on the innate immune system and provides novel mechanistic insights into the anti-inflammatory properties of these drugs.

9. Data suggest that SIK2 is critical in regulating whole-body glucose metabolism primarily by controlling the CRTC2-CREB function of the white adipocytes.

10. The SIK2-p35-PJA2 complex is essential for glucose homeostasis and provides a link between p35-CDK5 and the AMPK family in excitable cells.

11. tumor suppressor kinase LKB1 activates the downstream kinases SIK2 and SIK3 to stimulate nuclear export of class IIa histone deacetylases

12. These findings suggest that SIK2 plays critical roles in neuronal survival, is modulated by CaMK I/IV, and regulates CREB via TORC1.

13. SIK2 represses eumelanogenesis in mice.

14. low SIK2 activity was associated with increased p300 HAT activity, ChREBP hyperacetylation, and hepatic steatosis

15. Results support a role for SIK2 in adipocyte energy metabolism. SIK2 may function similarly to AMPK for turning off lipogenesis in low-energy state.

16. SIK2-TORC2 cascade may be important for the regulation of PGC-1alpha and UCP-1 gene expression in insulin signaling in brown adipose tissue