anti-Calnexin (CANX) Antikörper

Human Calnexin (CANX) Interaktionspartner

1. Study discovered that calnexin is highly abundant in human brain endothelial cells of multiple sclerosis (MS) patients. Conversely, mice lacking calnexin exhibited resistance to experimental autoimmune encephalomyelitis induction, no evidence of immune cell infiltration into the CNS. These findings identify a link between calnexin expression in CNS endothelial cells and neuroinflammation.

2. In summary, ER retention of pathogenic VLDLR mutants involves binding to calnexin, elevated endoplasmic reticulum stress, and delayed degradation which is dependent on SEL1L.

3. Increased tumour protein levels of calnexin may be of prognostic significance in colorectal cancer, and calnexin may represent a potential target for future therapies.

4. FUNDC1 integrates mitochondrial fission and mitophagy at the interface of the endoplasmic reticulum-mitochondrial contact site by working in concert with DRP1 and calnexin under hypoxic conditions in mammalian cells.

5. Results of further analyses by using a CNX mutant imply that ERp29 and ERp57 recognize the same domain of CNX, whereas the mode of interaction with CNX might be somewhat different between them.

6. Inhibit interaction between HIV-1 Nef and Calnexin to reverse HIV-induced lipid accumulation and prevent atherosclerosis.

7. Endogenous NOX4 forms macromolecular complexes with calnexin, which are needed for the proper maturation, processing, and function of NOX4 in the endoplasmic reticulum.

8. To study principles underlying dynamics and regulation of palmitoylation, the ER chaperone calnexin, which requires dual palmitoylation for function, was investigated.

9. These observations point at a previously unrecognized contribution of calnexin to the retention of NMT1 at the ER membrane.

10. Charcot-Marie-Tooth disease-related PMP22 is trapped in the endoplasmic reticulum by calnexin-dependent retention and Rer1-mediated early Golgi retrieval systems and partly degraded by the Hrd1-mediated endoplasmic reticulum-associated degradation system.

11. Data indicate that protein tyrosine phosphatase 1B (PTP1B) association with calnexin is ubiquitin conjugating enzyme 9 (UBC9)-dependent.

12. H-ERG trafficking was impaired by H2O2 after 48 h treatment, accompanied by reciprocal changes of expression between miR-17-5p seed miRNAs and several chaperones (Hsp70, Hsc70, CANX, and Golga20)

13. Nef regulates the activity of calnexin to stimulate its interaction with gp160 at the expense of ABCA1

14. The impact of CANX genetic variants to heart rate was discovered.

15. Soluble calnexin may fulfill functions similar to calreticulin.

16. calnexin tunes the cellular responses to epidermal growth factor receptor in a manner that depends on the health status of the endoplasmic reticulum

17. These findings demonstrated that calnexin strictly monitors the maturation of S protein by its direct binding, resulting in conferring infectivity on severe acute respiratory syndrome coronavirus.

18. The data suggest that patients with low or defective TAP1 or calnexin in primary breast cancers may be at higher risks for developing brain metastasis due to the defects in T cell-based immunosurveillance.

19. cysteine residues within calnexin are important for the structure and function of calnexin.

20. The findings showed that calnexin is a stable component of the ribosome-translocon complex in a manner that is exquisitely dependent on calnexin's palmitoylation status.

Mouse (Murine) Calnexin (CANX) Interaktionspartner

1. Study discovered that calnexin is highly abundant in human brain endothelial cells of multiple sclerosis (MS) patients. Conversely, mice lacking calnexin exhibited resistance to experimental autoimmune encephalomyelitis induction, no evidence of immune cell infiltration into the CNS. These findings identify a link between calnexin expression in CNS endothelial cells and neuroinflammation.

2. CNX has a specific role in cardiomyocyte viability and Ca(2+) cycling through its effects on endoplasmic reticulum stress, apoptosis and Ca(2+) channel expression.

3. Calnexin discriminates between different conformational states of GlyT2 displaying a lectin-independent chaperone activity.

4. calnexin and ERp57, but not calreticulin, play an important role in the biology of peripheral myelin proteins PMP22 and P0, and, consequently, these chaperones may contribute to the pathogenesis of peripheral neuropathies

5. Enhanced clathrin-dependent endocytosis in the absence of calnexin may contribute to the neurological phenotype of calnexin-deficient mice

6. Data show that the E351 mutation led to slightly enhanced ERp57 binding to calnexin, whereas W428 greatly enhanced binding of ERp57 to calnexin.

7. Suggest that Adam7 functions in fertilization through the formation of a complex with heat shock protein 5, calnexin and Itm2b during capacitation in sperm.

8. endoplasmic reticulum stress has effects on group VIA phospholipase A2 in beta cells that include tyrosine phosphorylation and increased association with calnexin

9. Calnexin deficiency leads to dysmyelination

10. Data give novel evidence that CyCAP regulates the post-translational modification of tissue transglutaminase through its colocalization with calnexin in endoplasmic reticulum.

11. Association with mutant peripheral myelin protein-22 ex vivo: a basis for "gain-of-function" ER diseases.

12. Calnexin is required for myelinated motor neuron function and postnatal survival in mice

13. Data show that in calreticulin-deficient cells, calnexin-substrate association is severely reduced, leading to accumulation of unfolded proteins and a triggering of the unfolded protein response.

14. caspase-3 or caspase-7 cleaves calnexin, whose cleaved product leads to the attenuation of apoptosis

15. Data show that oculocutaneous albinism soluble tyrosinase is an endoplasmic reticulum-associated degradation substrate that, unlike other albino tyrosinases, associates with calreticulin and BiP/GRP78, but not calnexin.

16. In mice, a calnexin-glycan interaction may be required to stabilize the weak association of MHC class I heavy chain with beta 2-microglobulin in the endoplasmic reticulum until peptide is bound.

17. UGT1 activity might be required for a structural maturation needed for substrate dissociation from calnexin and export from the ER.

18. Calnexin might stimulate the productive folding of WT CF transmembrane conductance regulator (CFTR), but not DeltaF508 CFTR, which has folding defects.

19. Cnx (-/-) cells have significantly increased proteasomal activity, which may play a role in the adaptive mechanisms addressing the acute endoplasmic reticulum stress observed in the absence of calnexin.

20. Mammalian rod opsin biogenesis does not appear to have an absolute requirement for Cnx.

Caenorhabditis elegans (C. elegans) Calnexin (CANX) Interaktionspartner

1. Loss-of-function mutations of cnx-1 decreased the protein level and current density of the UNC-103 K(+) channel and suppressed the behavioral defects caused by a gain-of-function mutation in unc-103 Moreover, CNX-1 facilitated tetrameric assembly of UNC-103 channel subunits in a liposome-assisted cell-free translation system.

Zebrafish Calnexin (CANX) Interaktionspartner

1. Results suggest that calnexin is essential for neuromast formation during lateral line development.