anti-Family with Sequence Similarity 134, Member B (FAM134B) Antibodies

Human Family with Sequence Similarity 134, Member B (FAM134B) interaction partners

1. Through molecular dynamic simulations of FAM134B in flat and curved membranes, we relate the dynamic RHD structure with its two wedge-shaped transmembrane helical hairpins and two amphipathic helices to FAM134B functions in membrane-curvature induction and curvature-mediated protein sorting.

2. This study has first time reported the gene signaling networks with which FAM134B interacts and noted that FAM134B is involved in the regulation of WNT/beta-catenin pathway by EB1-mediated modulating of APC in colon cancer cells.

3. the expression level of JK-1 is correlated with the clinicopathological features of esophageal carcinoma

4. FAM134B promoter methylation plays a key role in regulating FAM134B expression in vitro and in vivo, which in turn contributes to the prediction of the biological aggressiveness of colorectal adenocarcinomas.

5. These findings imply that mutation might be the major driving source of FAM134B genetic modulation in oesophageal squamous cell carcinoma.

6. NS3-mediated cleavage of FAM134B blocks the formation of endoplasmic reticulum and viral protein-enriched autophagosomes.

7. miR-186-5p expression promotes colorectal cancer pathogenesis by regulating tumour suppressor FAM134B

8. FAM134B protein was noted in both cytoplasm and nuclei of colon cancer cells. In cancer cells derived from stage IV colon cancer, FAM134B expression was remarkably reduced when compared to non-cancer colon cells and cancer cells derived from stage II colon cancer. FAM134B knockdown significantly (P < 0.05) increased the proliferation of colon cancer cells following lentiviral transfection.

9. FAM134B mutation is common in colorectal cancer. The association of the mutation of this gene with adverse clinical and pathological parameters is congruent with the tumour suppressive properties of the gene

10. selective endoplasmic reticulum (ER)-phagy via FAM134 proteins is indispensable for mammalian cell homeostasis and controls ER morphology and turnover in mice and humans

11. The changes in JK1 DNA copy number associated with progression of colorectal neoplasms.A decrease in JK-1 copy number was correlated with a shorter disease-free survival time.

12. FAM134B represses cell migration in colon cancer.FAM134B has functional role in the pathogenesis of colon cancer.

13. Low FAM134B expression is associated with colorectal cancer.

14. Results show the interplay between promoter SNPs of CD39 and FAM134B results in an intercellular epistasis which influences the risk of a complex inflammatory disease.

15. Homozygous FAM134B mutation was found in Turkish siblings with hereditary sensory neuropathy type 2.

16. case report of homozygous nonsense mutation p.Q145X causing severe hereditary sensory neuropathy

17. The FAM134B and TNFRSF19 showed a dramatically strong synergistic epistasis in explaining the genetic dissection of the susceptibility to complex vascular dementia.

18. The overexpression of JK-1(FAM134b) and its transforming capacity in normal cells may play a critical role in the molecular pathogenesis of esophageal squamous cell carcinoma.

19. show that loss-of-function mutations in FAM134B, encoding a newly identified cis-Golgi protein, cause hereditary sensory and autonomic neuropathy type II.

Mouse (Murine) Family with Sequence Similarity 134, Member B (FAM134B) interaction partners

1. FAM134B-dependent endoplasmic reticulum (ER)-phagy is an important limiting event in Ebola virus (EBOV) replication in mouse cells

2. selective endoplasmic reticulum (ER)-phagy via FAM134 proteins is indispensable for mammalian cell homeostasis and controls ER morphology and turnover in mice and humans

3. show that loss-of-function mutations in FAM134B, encoding a newly identified cis-Golgi protein, cause hereditary sensory and autonomic neuropathy type II.