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Cofactor E is one of four proteins (cofactors A, D, E, and C) involved in the pathway leading to correctly folded beta-tubulin from folding intermediates. Additionally we are shipping TBCE Antibodies (85) and TBCE Kits (9) and many more products for this protein.
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This study reported that reduced expression of the tubulin (show TUBB Proteins)-specific chaperone TBCE leads to defective microtubule polymerization and impaired microtubule-dependent axonal transport in sensory DRG neurons of pmn mice.
ARF1 (show ARF1 Proteins)/TBCE-mediated cross-talk that coordinates COPI formation and tubulin (show TUBB Proteins) polymerization at the Golgi.
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
Tbce is critical for the maintenance of microtubules in mouse motor axons
TBCE protein was localized in the middle region and in the tail of the sperm while in the oocyte the localization was cytosolic.
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
Sanjad-Sakati syndrome molecular pathology has been shown to be due to mutations in the TBCE gene on chromosome 1q42-q43.
the role of the human TBCE and TBCB (show TBCB Proteins) chaperones in alpha-tubulin (show TUBA4A Proteins)-beta-tubulin (show TUBB Proteins) dissociation, was investigated.
tudies confirmed elevated expression of three target antigens RAB38, TBCE, and DUSP12 in CML.
TBCE has a role in membrane trafficking in the Golgi and late endosomal compartments, tubulin (show TUBB Proteins) assembly, and the development of the parathyroid
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.
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.
TBCE, TBCB (show TBCB Proteins) and alpha-tubulin (show TUBA4A Proteins) form a ternary complex after heterodimer dissociation. These complexes might serve to escort alpha-tubulin (show TUBA4A Proteins) towards degradation or recycling, depending on the cell requirements.
Cofactor E is one of four proteins (cofactors A, D, E, and C) involved in the pathway leading to correctly folded beta-tubulin from folding intermediates. Cofactors A and D are believed to play a role in capturing and stabilizing beta-tubulin intermediates in a quasi-native confirmation. Cofactor E binds to the cofactor D/beta-tubulin complex\; interaction with cofactor C then causes the release of beta-tubulin polypeptides that are committed to the native state. Two transcript variants encoding the same protein have been found for this gene.
progressive motor neuropathy
, tubulin-folding cofactor E
, Kenny-Caffey syndrome
, tubulin-specific chaperone E
, beta-tubulin cofactor E