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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 Proteins (6) and TBCE Kits (4) and many more products for this protein.
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Human Polyclonal TBCE Primary Antibody for WB - ABIN520724
Bellouze, Schäfer, Buttigieg, Baillat, Rabouille, Haase: Golgi fragmentation in pmn mice is due to a defective ARF1/TBCE cross-talk that coordinates COPI vesicle formation and tubulin polymerization. in Human molecular genetics 2014
Human Polyclonal TBCE Primary Antibody for ICC, IF - ABIN4358010
Sferra, Baillat, Rizza, Barresi, Flex, Tasca, DAmico, Bellacchio, Ciolfi, Caputo, Cecchetti, Torella, Zanni, Diodato, Piermarini, Niceta, Coppola, Tedeschi, Martinelli, Dionisi-Vici, Nigro et al.: TBCE Mutations Cause Early-Onset Progressive Encephalopathy with Distal Spinal Muscular Atrophy. ... in American journal of human genetics 2016
ARF1 (show ARF1 Antibodies)/TBCE-mediated cross-talk that coordinates COPI formation and tubulin (show TUBB Antibodies) 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
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 Antibodies) chaperones in alpha-tubulin (show TUBA4A Antibodies)-beta-tubulin (show TUBB Antibodies) 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 Antibodies) 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 Antibodies) and alpha-tubulin (show TUBA4A Antibodies) form a ternary complex after heterodimer dissociation. These complexes might serve to escort alpha-tubulin (show TUBA4A Antibodies) towards degradation or recycling, depending on the cell requirements.
Depletion of Op18 (show STMN1 Antibodies) by means of RNA interference increased the susceptibility of tubulin (show TUBB Antibodies) to TBCE or E-like (show TBCEL Antibodies) mediated disruption, while overexpressed Op18 (show STMN1 Antibodies) exerted a tubulin (show TUBB Antibodies)-protective effect.
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