anti-Trafficking Protein Particle Complex 9 (TRAPPC9) Antibodies

Human Trafficking Protein Particle Complex 9 (TRAPPC9) interaction partners

1. CNVs significantly contribute to the mutational spectrum of TRAPPC9 gene associated with syndromic intellectual disability.

2. Data show that NIBP expression level is high in gastric cancer (GC) patients and indicate that the NIBPregulated NFkappaB signaling pathway plays a pivotal role in the chemoresistance of GC cells by promoting EMT.

3. Homozygous TRAPPC9 gene nonsense mutation in OXTR gene is associated with intellectual disability, speech disorder, and secondary microcephaly.

4. In this study, we report that WES analysis allowed identification of the causal molecular lesion in both patients. In the first family of Egyptian origin, a homozygous nonsense mutation (c.1423C>T; p.Arg377*) in TRAPPC9 was identified

5. In conclusion, we demonstrated that NIBP knockdown reduces colorectal cancer metastasis through down-regulation of canonical NF-kappaBeta signaling and suppression of ERK and JNK signaling.

6. NIBP impacts on the expression levels of Ecadherin, CD44 and vimentin via the NFkappaB classical and alternative pathways.

7. NIBP reflects a higher metastatic potential of CRC tumors, and its mechanism of action may be through regulation of the classical NF-kappaB pathway and increased MMP-2 and MMP-9 expression

8. Data identified important roles of NIBP in promoting tumorigenesis via NFkappaBeta signaling.

9. Identification and construction of a 3D protein model of trafficking protein particle complex 9 (TRAPPC9), a potetnially interesting molecular target for the development of drug therapy against non syndromic mental retardation

10. By detailed phenotypic analysis of our patients, and by critical literature review, we found that homozygous TRAPPC9 loss-of-function mutations cause a distinctive phenotype, characterized by peculiar facial appearance, obesity, hypotonia

11. A homozygous splice site mutation in TRAPPC9 causes intellectual disability and microcephaly.

12. Data suggest that TRAPPC9 serves to uncouple p150(Glued) from the COPII coat, and to relay the vesicle-dynactin interaction at the target membrane.

13. Data show that a disease-causing mutation of TRAPPC2, D47Y, failed to interact with either TRAPPC9 or TRAPPC8, suggesting that aspartate 47 in TRAPPC2 is at or near the site of interaction with TRAPPC9 or TRAPPC8.

14. Studies indicate that a truncation of TRAPPC9 leads to mental retardation.

15. TRAPPC9 has a role in brain development, possibly through its effect on NF-kappaB activation and protein trafficking in the postmitotic neurons of the cerebral cortex

16. TRAPPC9, encodes the NIK- and IKK-beta-binding protein, has a role in nonsyndromic autosomal-recessive mental retardation

17. NIBP is a NIK and IKK(beta)-binding protein that enhances NF-(kappa)B activation

Mouse (Murine) Trafficking Protein Particle Complex 9 (TRAPPC9) interaction partners

1. NIBP is extensively expressed in the enteric nervous system with relatively high level in a subpopulation of enteric neurons.

2. Data show Trs130 (mTrs130) is a component of an analogous TRAPP complex that this complex is enriched on COPI (Coat Protein I)-coated vesicles it specifically activates Rab1.

3. TRAPPC9 has a role in brain development, possibly through its effect on NF-kappaB activation and protein trafficking in the postmitotic neurons of the cerebral cortex

4. NIBP is a NIK and IKK(beta)-binding protein that enhances NF-(kappa)B activation.

5. IBP, a novel regulator of Rho GTPases, is required for optimal T cell effector function, lymphocyte homeostasis, and the prevention of systemic autoimmunity.

Cow (Bovine) Trafficking Protein Particle Complex 9 (TRAPPC9) interaction partners

1. The minimal residues of NIBP that interact with NS5A of bovine viral diarrhea virus were mapped as aa 597-623.