anti-Tubulin Folding Cofactor E (TBCE) Antibodies

Mouse (Murine) Tubulin Folding Cofactor E (TBCE) interaction partners

1. This study reported that reduced expression of the tubulin-specific chaperone TBCE leads to defective microtubule polymerization and impaired microtubule-dependent axonal transport in sensory DRG neurons of pmn mice.

2. ARF1/TBCE-mediated cross-talk that coordinates COPI formation and tubulin polymerization at the Golgi.

3. We conclude from our study that the mutation of the TBCE gene affects the auditory nerve and the cochlear hair cells simultaneously, leading to progressive hearing loss

4. Tbce is critical for the maintenance of microtubules in mouse motor axons

Human Tubulin Folding Cofactor E (TBCE) interaction partners

1. Mutation analysis of the TBCE gene revealed the common 12-bp (155-166del) deletion in three new Sanjad-Sakati syndrome patients from Tunisia.

2. TBCE protein was localized in the middle region and in the tail of the sperm while in the oocyte the localization was cytosolic.

3. Although loss of function of TBCE has been documented to impact multiple developmental processes, the present findings provide evidence that hypomorphic TBCE mutations primarily drive neurodegeneration

4. Sanjad-Sakati syndrome molecular pathology has been shown to be due to mutations in the TBCE gene on chromosome 1q42-q43.

5. the role of the human TBCE and TBCB chaperones in alpha-tubulin-beta-tubulin dissociation, was investigated.

6. tudies confirmed elevated expression of three target antigens RAB38, TBCE, and DUSP12 in CML.

7. TBCE has a role in membrane trafficking in the Golgi and late endosomal compartments, tubulin assembly, and the development of the parathyroid

8. Tbce is critical for the maintenance of microtubules in mouse motor axons

9. The tubulin-specific chaperone E (Tbce) mutation described here suggests that alterations in tubulin assembly lead to retrograde degeneration of motor axons, ultimately resulting in motoneuron cell death.

10. Reviews recent findings on the molecular mechanisms of the development of the parathyroid glands, with special emphasis on the possible role of tubulin chaperone E (TBCE), implicated in the hypopathyroidism, retardation and dysmorphism (HRD) syndrome.

11. TBCE, TBCB and alpha-tubulin form a ternary complex after heterodimer dissociation. These complexes might serve to escort alpha-tubulin towards degradation or recycling, depending on the cell requirements.

12. Depletion of Op18 by means of RNA interference increased the susceptibility of tubulin to TBCE or E-like mediated disruption, while overexpressed Op18 exerted a tubulin-protective effect.

13. Study demonstrates that, unlike its counterpart TBCE, TBCB only moderately destabilizes microtubules.

14. TBCE is required for the normal development and function of neuromuscular synapses and that it promotes microtubule formation

15. TBCE may play a role in development of the anterior pituitary, corpus callosum, and white matter in addition to the parathyroid glands.