anti-Vacuolar Protein Sorting 33 Homolog B (Yeast) (VPS33B) Antibodies

Fruit Fly (Drosophila melanogaster) Vacuolar Protein Sorting 33 Homolog B (Yeast) (VPS33B) interaction partners

1. this study shows that Vps33B function is critical for determining the fate of signaling endosomes formed following pattern-recognition receptors activation

Human Vacuolar Protein Sorting 33 Homolog B (Yeast) (VPS33B) interaction partners

1. ARKID syndrome is caused by VPS33B mutation.

2. Vesicular trafficking complexes, containing VPS33B, are a novel class of modifiers of integrin function.

3. Novel splice site mutations in the VPS33B gene were identified in arthrogryposis, renal dysfunction, and cholestasis syndrome in Koreans.

4. Abnormal protein trafficking and impairment in multivesicular bodies maturation in Megakaryocytes underlie the alpha-granule deficiency in Vps33b(fl/fl)-ER(T2) mouse and ARC patients.

5. Case Report: neonate with ARC syndrome and high GGT cholestasis caused by VPS33B heterozygous mutations.

6. Case Report: novel mutations in VPS33B in Chinese patient with arthrogryposis, renal dysfunction and cholestasis syndrome.

7. Our data suggest that the ARC syndrome may result through impaired VIPAS39/SPE-39 and Vps33b-dependent endosomal maturation or fusion.

8. Evidence of genotype-phenotype correlation in ARC syndrome the VPS33B c.1225+5G>C mutation predicts a mild phenotype.

9. VPS16B, similar to its binding partner VPS33B, is essential for megakaryocyte and platelet alpha-granule biogenesis.

10. SPE-39 due to tyrosine phosphorylation and ubiquitination on the function of Vps33B in the EGF-stimulated cells

11. encodes a homolog of the class C yeast vacuolar protein sorting gene, that contains a Sec1-like domain important in the regulation of vesicle-to-target SNARE complex formation and subsequent membrane fusion

12. A and B classes reflect the evolution of organelle/tissue-specific functions

13. VPS33B is involved in intracellular vesicle trafficking

14. The present observations indicate that VPS33B deficiency results in abnormal secretion of lamellar granules, which underlies ichthyosis in ARC syndrome.

15. Genetic deletion of ptpA attenuates Mycobacterium tuberculosis growth in human macrophages and identify VPS33B, a regulator of membrane fusion, as a PtpA substrate.

16. We assessed the clinical characteristics and investigated the VPS33B mutations in Korean patients with ARC (arthrogryposis, renal dysfunction, and cholestasis) syndrome.

Zebrafish Vacuolar Protein Sorting 33 Homolog B (Yeast) (VPS33B) interaction partners

1. knockdown of atp6ap2 and vps33b had an additive negative effect on biliary development.

2. findings identify vps33b is a novel downstream target gene of the hnf6/vhnf1 pathway that regulates bile duct development in zebrafish

Mouse (Murine) Vacuolar Protein Sorting 33 Homolog B (Yeast) (VPS33B) interaction partners

1. VPS33B and VIPAR are essential for epidermal lamellar body biogenesis and function

2. VPS33B is vital for maintenance of mammalian structural and functional hepatocyte polarity.

3. this study shows that Vps33B is required in mouse macrophages for normal maturation of phagosomes and specialized endosomes that are induced upon pattern-recognition receptors activation

4. VPS33B interacted with the GDI2/RAB11A/RAB27A pathway to regulate the trafficking of secretory proteins as exosomes.

5. The data presented in this study suggest that Vps33b is involved in alpha-granule formation possibly by facilitating the Vwf-positive vesicular trafficking to alpha-granule-related vacuoles in megakaryocytes.

6. Abnormal protein trafficking and impairment in multivesicular bodies maturation in Megakaryocytes underlie the alpha-granule deficiency in Vps33b(fl/fl)-ER(T2) mouse and ARC patients.