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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. Zusätzlich bieten wir Ihnen TBCE Kits (7) und TBCE Proteine (6) und viele weitere Produktgruppen zu diesem Protein an.
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Human Polyclonal TBCE Primary Antibody für 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 für 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
This study reported that reduced expression of the tubulin (zeige TUBB Antikörper)-specific chaperone TBCE leads to defective microtubule polymerization and impaired microtubule-dependent axonal transport in sensory DRG neurons of pmn mice.
ARF1 (zeige ARF1 Antikörper)/TBCE-mediated cross-talk that coordinates COPI formation and tubulin (zeige TUBB Antikörper) 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 (zeige TBCB Antikörper) chaperones in alpha-tubulin (zeige TUBA4A Antikörper)-beta-tubulin (zeige TUBB Antikörper) 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 (zeige TUBB Antikörper) 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 (zeige TBCB Antikörper) and alpha-tubulin (zeige TUBA4A Antikörper) form a ternary complex after heterodimer dissociation. These complexes might serve to escort alpha-tubulin (zeige TUBA4A Antikörper) 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