CD5 Molecule-Like (CD5L) ELISA Kits

Human CD5 Molecule-Like (CD5L) Interaktionspartner

1. this study shows that CD5L promotes M2 macrophage polarization through autophagy-mediated upregulation of ID3

2. CD5L is upregulated in hepatocellular carcinoma. CD5L promotes liver cancer cell proliferation and antiapoptotic responses by binding to HSPA5.

3. Low serum AIM levels in patients who have previously experienced peritoneal dialysis-related peritonitis.

4. Taken together with our results on the aberrant ex vivo production of CD5L, this study has provided new evidence for the potential immunopathological role of CD5L in the exacerbation of SLE disease, and circulating concentration of CD5L may act as a potential disease marker for the monitoring of disease severity and therapeutic effects in SLE patients.

5. AIM enhances intratubular debris clearance and ameliorates acute kidney injury via interaction with KIM-1.

6. The present study provides the first evidence that apoptosis inhibitor of macrophages binds to IGFBP2, 3 and 4.

7. CD36 is involved in autophagy; the CD5L-CD36 axis has a role in the induction of macrophage autophagy

8. CD5L is a key protein in the control of immune homeostasis and inflammatory disease. (Review)

9. Apoptosis inhibitor of macrophage levels were markedly higher in patients with advanced liver damage, regardless of disease type, and correlated significantly with multiple parameters representing liver function.

10. AIM contributes to key macrophage responses to M. tuberculosis

11. Our data represent the first evidence that human AIM is involved in macrophage survival, adhesion, and foam cell formation

12. N-glycosylation plays important roles in the secretion and lipolytic function of AIM

13. AIM is involved in the progression of MetS in both an advancing and inhibitory fashion. Regulation of AIM could therefore be therapeutically applicable for MetS.

14. Spalpha is an active constituent of the innate immune response of the host

15. CD5L and ApoE were significantly up-regulated or down-regulated, respectively, in the plasma from AD patients compared with that from healthy donors.

16. Dysregulation of myeloid cell populations by extracellular transgene Api6 signaling leads to abnormal myelopoiesis and lung cancer in bitransgenic mice.

Mouse (Murine) CD5 Molecule-Like (CD5L) Interaktionspartner

1. AIM appears to be involved in the prevention and repair process of a peritoneal dialysis-related fungal peritonitis.

2. AIM/CD5L-deficient mice demonstrated a smaller infarct size and less of an inflammatory response via inflammatory pathways after myocardial infarction; these data provide the first evidence that AIM/CD5L plays an important role in the inflammatory responses after myocardial injury

3. AIM enhances intratubular debris clearance and ameliorates acute kidney injury via interaction with KIM-1.

4. CD5L as a critical regulator that distinguishes Th17 functional states and identified T cell lipid metabolism as an integral component of the pathways regulating Th17 cell pathogenicity.

5. plays a general homeostatic role by supporting innate immunity during pathogen aggression

6. the assembled p40-CD5L heterodimer does not recapitulate the biological activity of IL-12.

7. AIM contributes to key macrophage responses to M. tuberculosis

8. AIM-IgM association plays a critical role in the obesity-associated autoimmune process.

9. SREBP-1a specifically activates the Api6 gene through a binding site in its proximal promoter, thus establishing the Api6 gene as a newly identified SREBP-1a target gene

10. N-glycosylation plays important roles in the secretion and lipolytic function of AIM

11. AIM induces lipolysis in a manner distinct from that of hormone-dependent lipolysis, without activation or augmentation of lipases.

12. Apoptosis inhibitor of macrophage (AIM) is required for obesity-associated recruitment of inflammatory macrophages into adipose tissue.

13. AIM binds to cytosolic FAS protein at various regions responsible for elongation of fatty acids, release of synthesized palmitate, and stabilization of FAS dimerization.

14. The protein inhibits apoptosis of T cells and NKT cells in Corynebacterium-induced granuloma formation in mice.

15. Api6 production facilitates macrophage survival within atherosclerotic lesions and that loss of Api6 decreases early lesion development by increasing macrophage apoptosis

16. Bacterial lipoteichoic acid might affect the pathogenesis of epithelial inflammation followed by fibrosis in systemic multifocal epithelial inflammations in chronic colitis-harboring TCR alpha(-/-) x AIM(-/-) mice