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the component proteins of the machinery, OSBP (显示 OSBP 抗体), VAP (显示 F10 抗体), SAC1 (显示 SACM1L 抗体), and PITPNB (显示 PITPNB 抗体), are all essential host factors for AiV (显示 ANXA4 抗体) replication. Importantly, the machinery is directly recruited to the RNA replication sites through previously unknown interactions of VAP (显示 F10 抗体)/OSBP (显示 OSBP 抗体)/SAC1 (显示 SACM1L 抗体) with the AiV (显示 ANXA4 抗体) proteins and with ACBD3 (显示 Acbd3 抗体).
Lifelong elevation of neuronal VAPB slowed the decline of neurological impairment, delayed denervation of hindlimb muscles, and prolonged survival of spinal motor neurons.
Study showed that alpha-synuclein perturbs endoplasmic reticulum-mitochondria associations and that this involves disruption to the VAPB-PTPIP51 (显示 FAM82A2 抗体) tethering proteins. Using a range of assays including immunoprecipitation, cellular glutathione S-transferase (显示 GSTa2 抗体) pull-down, proximity ligation and in vitro binding of recombinant proteins, study showed that alpha-synuclein is a direct binding partner for VAPB.
ACBD5 (显示 ACBD5 抗体)-VAPB interaction regulates peroxisome-endoplasmic reticulum associations. Loss of PO-ER association perturbs PO membrane expansion and increases PO movement.
VAP (显示 F10 抗体)-ACBD5 (显示 ACBD5 抗体)-mediated contact between the endoplasmic reticulum and peroxisomes mediate organelle maintenance and lipid homeostasis.
Effects of the combined absence of VAPA (显示 VAPA 抗体) and VAPB in human cells were studied; cells lacking VAP (显示 F10 抗体) accumulate high levels of PI4P, actin comets, and trans-Golgi proteins on endosomes. Such defects are mimicked by downregulation of OSBP (显示 OSBP 抗体), a VAP (显示 F10 抗体) interactor and PI4P transporter that participates in VAP (显示 F10 抗体)-dependent endoplasmic reticulum-endosomes tethers.
this is the first study to report Amyotrophic lateral sclerosis caused by a VAPB mutation in a Chinese population.
Our work revealed that VAP-A/B knockdown impaired the processing and secretion of PAUF, which is one of the cargo proteins of carriers of the trans-Golgi network to the cell surface.
Heterozygous P56S Vapb knock-in mice show mild age-dependent defects in motor behaviors as characteristic features of the disease. The homozygous P56S Vapb knock-in mice show more severe defects compared with heterozygous mice reflecting the dominant and dose-dependent effects of P56S mutation.
VAPB inhibited the degradation of DeltaF508-CFTR in the ER through interactions with the RMA1-Derlin-BAP31-VCP pathway.
To identify pathological defects in animals expressing the P56S mutant VAPB protein at physiological levels in the appropriate tissues, we have generated Vapb knock-in mice
The disruption of the IRE1 (显示 ERN1 抗体)-XBP1 (显示 XBP1 抗体) pathway is a cause for the reduced myotube formation in P56S-VAPB-mutation expressing cells.
Vapb knock-out mice exhibit abnormal muscular triacylglycerol levels and FoxO (显示 FOXO3 抗体) target gene transcriptional responses to fasting and refeeding
Mice knocked-out for Vapb showed mild motor deficits after 18 months of age.
VapB positively regulates RANKL (显示 TNFSF11 抗体)-mediated osteoclastogenesis via PLCgamma2 (显示 PLCG2 抗体)-Ca(2 (显示 CA2 抗体)+)-NFAT (显示 NFATC1 抗体) signaling
Co-expression of mutant protein-associated protein B (显示 LEPREL2 抗体) (VAPB) enhances the transactive response DNA-binding protein (显示 HSF4 抗体)-43 (TDP-43 (显示 TARDBP 抗体))-induced motor neuronal cell death while that of wild type-VAPB attenuates it.
Adeno (显示 ADORA2A 抗体)-associated viral-mediated over-expression of both wild-type and mutated form of human VAPB selectively induces death of primary motor neurons, albeit with different kinetics.
However, VAPBP56S but not VAPBwt transgenic mice develop cytoplasmic TDP-43 (显示 TARDBP 抗体) accumulations within spinal cord motor neurons that were first detected at 18 months of age.
The total loss of VAPB function in unfolded protein response, induced by one P56S mutant allele, may contribute to the development of P56SVAPB- induced amyotrophic lateral sclerosis.
The protein encoded by this gene is a type IV membrane protein found in plasma and intracellular vesicle membranes. The encoded protein is found as a homodimer and as a heterodimer with VAPA. This protein also can interact with VAMP1 and VAMP2 and may be involved in vesicle trafficking.
VAMP-associated 33 kDa protein
, vesicle-associated membrane protein-associated protein B/C
, VAMP (vesicle-associated membrane protein)-associated protein B and C
, VAMP-associated protein B/C
, VAMP-associated protein B
, vesicle-associated membrane protein, associated protein B and C
, vesicle-associated membrane protein-associated protein B
, VAMP-associated protein 33b
, VAMP (vesicle-associated membrane protein)-associated protein B and C L homeolog