anti-Fatty Acid Binding Protein 5 (Psoriasis-Associated) (FABP5) Antibodies

Human Fatty Acid Binding Protein 5 (Psoriasis-Associated) (FABP5) interaction partners

1. FABP5 promotes the budding of particles approximately 150 nm in diameter and modulates the kinetics of the SAR1 GTPase cycle.

2. FABP5 might promote the carcinogenesis and metastasis of cervical cancer via up-regulating MMP-2 and MMP-9.

3. The E-FABP concentration in tears appears to be related to ocular surface epithelial damage and tear stability in patients with dry eye disease in Sjogren syndrome.

4. FABP5 promotes tumor angiogenesis via activation of the IL6/STAT3/VEGFA signaling pathway in hepatocellular carcinoma.

5. FABP5 promotes lipolysis of lipid droplets, de novo fatty acid synthesis and activation of NF-kappaB signaling in cancer cells.

6. Although FABP5 facilitates brain endothelial cell uptake of fatty acids, it has limited effects on brain endothelial cell uptake.

7. Results show that circulating FABP5 is associated with decreased cholesterol efflux capacity (CEC) and carotid atherosclerosis, suggesting that FABP5 level is a regulatory factor of CEC and a potential biomarker for residual risk of atherosclerosis.

8. Compared to control group, breast cancer patients show higher FABP4 and FABP5 blood levels. Our data suggest that, particularly, circulating FABP4 levels could be considered a new independent breast cancer biomarker. Our work translates basic science data to clinic linking the relationship between adipose tissue and lipid metabolism to breast cancer.

9. the critical role of FABP5 in activating the TGF-beta signaling pathway during radiation-induced human skin fibrosis

10. Study identified FABP5 to be involved in the progressive intestinal injury associated with the development of Crohn's Disease complications via their effects on intestinal innate immunity.

11. Findings show that FABP5 expression is up-regulated in hepatocellular carcinoma (HCC), and provide evidence that that it could play a crucial role of tumor progression, invasion and metastasis in HCC through EMT induction.

12. Circulating levels of AFABP and EFABP are not decreased in Lipodystrophy despite adipose tissue loss in contrast to other adipokines including leptin and adiponectin.

13. A high expression ratio between FABP5 and CRABPII may be related to CP tumor recurrence and ATRA could be a potential therapeutic agent for CP chemotherapy.

14. Data suggest that antinociceptive agent SBFI-26 binds at a portal site as well as at the canonical site in the substrate pocket of FABP5 and FABP7; only the S form of SBFI-26 binds to both FABP5 and FABP7 in their co-crystal structures; SBFI-26 induces conformational changes in FABP5 and FABP7.

15. secreted FABP4 and FABP5 from adipocytes as adipokines differentially affect transcriptional and metabolic regulation in ADSC near adipocytes

16. FABP5 plays an important role in the carcinogenesis and metastasis of cervical cancer, and FABP5 may be a novel predictor for prognostic assessment of cervical cancer patients.

17. FABP5 promoted VEGF expression and angiogenesis through PPARgamma which was activated by fatty acids transported by FABP5.

18. FABP5 is associated with increased subclinical atherosclerosis

19. the balance between FABP4 and FABP5 in endothelial cells may be important in regulation of angiogenic versus quiescent phenotypes in blood vessels.

20. Long chain fatty acids suppress the oncogenic properties of FABP5-expressing carcinoma cells in cultured cells.

Mouse (Murine) Fatty Acid Binding Protein 5 (Psoriasis-Associated) (FABP5) interaction partners

1. The findings of this study suggest that genetic deletion, but not pharmacological inhibiton, of FABP5 affects sucrose intake and antidepressant-related behavior.

2. FABP4/5 have crucial roles in nutrient homeostasis during prolonged fasting for maintaining exercise endurance capacity.

3. our data suggest an unknown function of E-FABP in prevention of skin tumor development, and offer E-FABP as a therapeutic target for improving skin innate immunity in chemical-induced skin tumor prevention.

4. This study demonstrated the role of FABPs may play an important role in drug-seeking behavior under stressful conditions.

5. Fabp4/5 confers protection against metabolic diseases but does not extend lifespan.

6. Lack of PPARbeta/delta-expression, TUNEL reaction, RA receptor (RAR)beta, and cellular retinoic acid-binding protein (CRABP)-II were induced in E-FABP-positive septoclasts under RA excess, suggesting the growth arrest/cell-death of septoclasts, whereas cartilage-derived retinoic acid-sensitive protein (CD-RAP) inducing the cell growth arrest or morphological changes was induced in septoclasts under VA deficiency.

7. A 42.1 +/- 12.6% decrease in the BBB transport of (14) C-DHA in 8-month-old AD transgenic mice relative to wild-type mice was associated with a 34.5 +/- 6.7% reduction in FABP5 expression in isolated brain capillaries. Short-term spatial and recognition memory deficits were seen in AD mice on a 6-month n-3 fatty acid-depleted diet, but not those on control diet.

8. Using a yeast two-hybrid screen, immunoprecipitation, microscale thermophoresis analysis and cellular fractionation, we discovered that Fabp5 interacts with the calnexin cytoplasmic C-tail domain at the endoplasmic reticulum. These observations identify Fabp5 as a previously unrecognized calnexin binding partner.

9. Following infection with Listeria monocytogenes, we observed similar clonal expansion, contraction and formation of memory CD8 T cells in WT and E-FABP-/- mice. Analysis of Listeria-specific CD4 T cells revealed no defect in the expansion, contraction, and formation of memory CD4 T cells in E-FABP-/- mice. Our data demonstrate that E-FABP is dispensable for antigen-specific T cell response following bacterial infection.

10. Genetic deletion of fatty acid-binding protein 5 (FABP5) in mice reduces uptake of exogenous docosahexaenoic acid (DHA) into brain endothelial cells and brain capillaries and reduces brain parenchymal levels of endogenous DHA. Therefore, FABP5 in the brain endothelial cell is a crucial contributor to the brain levels of DHA. Critically, lowered brain DHA levels in FABP5(-/-) mice occurred in tandem with cognitive deficits

11. the balance between FABP4 and FABP5 in endothelial cells may be important in regulation of angiogenic versus quiescent phenotypes in blood vessels.

12. Mice lacking FABP5 and FABP7, which exhibit highest affinities for endocannabinoids, possessed elevated levels of the endocannabinoid anandamide and the related N-acylethanolamines palmitoylethanolamide and oleoylethanolamide.

13. These studies show, for the first time, a correlation between FABP5 and EGFR in enhancing TNBC metastasis through a novel mechanism

14. loss of FABP5 promotes a more anti-inflammatory response.

15. Circulating levels of GIP were significantly decreased in FABP5-deficient mice.

16. The frameshift and missense mutations in FABP3, FABP5, and FABP7 genes have been identified in schizophrenia and autism spectrum disorder in humans and in mouse behavioral studies.

17. FABP5 contributes to the development of Diet-induced obesity in a gastric inhibitory polypeptide-dependent manner.

18. Data indicate that epidermal fatty acid binding protein (E-FABP)-immunoreactivity was found in the entire cytoplasm and on the mitochondrial outer membrane.

19. FABP4/5 play an indispensable role in thermogenesis in brown adipose tissue and skeletal muscle.

20. FABP7 and FABP5 are differentially expressed in oligodendrocyte lineage cells and regulate their proliferation and/or differentiation.

Pig (Porcine) Fatty Acid Binding Protein 5 (Psoriasis-Associated) (FABP5) interaction partners

1. FABP4 gene expression level in adipose tissue was higher than in muscle. In contrast, FABP5 was expressed at low levels in adipocytes and muscle tissues. Low and moderate correlations between FABP4 and FABP5 gene expression were observed in muscle and in backfat, respectively.

2. QTL and haplotype analysis revealed that both FABP4 and FABP5 (clustered in mammals) are major candidate genes for the FAT1 QTL; the most likely position for the FAT1 QTL is between these two genes.