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Unc-13 homolog B

Munc13, Munc13-2, Hmunc13
This gene is expressed in the kidney cortical epithelial cells and is upregulated by hyperglycemia. The encoded protein shares a high level of similarity to the rat homolog, and contains 3 C2 domains and a diacylglycerol-binding C1 domain. Hyperglycemia increases the levels of diacylglycerol, which has been shown to induce apoptosis in cells transfected with this gene and thus contribute to the renal cell complications of hyperglycemia. Studies in other species also indicate a role for this protein in the priming step of synaptic vesicle exocytosis. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Munc13-4, Perforin, HAD, CAN, FHL2
Papers using Munc13 antibodies
Piccolo modulation of Synapsin1a dynamics regulates synaptic vesicle exocytosis
Garner Craig C. et al., In The Journal of Cell Biology, 2003
... GFP antibody from Roche, neomycin antibody from GeneTex, Inc., α-tubulin antibodies from Sigma-Aldrich, RIM1α and Munc13 from Synaptic Systems GmbH, PSD-95 from Affinity ...
Molecular dissection of the photoreceptor ribbon synapse
Brandstätter Johann H. et al., In The Journal of Cell Biology, 1996
... blot [WB] 1:5,000) and anti-CtBP2 mAbs (post-EM 1:1,000; IHC 1:10,000; WB 1:5,000; BD Biosciences), rabbit anti-pan-Munc13 pAb (WB 1:250; BD Biosciences), mouse anti-RIM mAb (WB ...
Papers on Munc13
Fast cerebellar reflex circuitry requires synaptic vesicle priming by munc13-3.
Ehrenreich et al., Göttingen, Germany. In Cerebellum, Jun 2015
Munc13-3 is a member of the Munc13 family of synaptic vesicle priming proteins and mainly expressed in cerebellar neurons.
Patients with Griscelli syndrome and normal pigmentation identify RAB27A mutations that selectively disrupt MUNC13-4 binding.
Aricò et al., Florence, Italy. In J Allergy Clin Immunol, May 2015
All 6 patients carried mutations at amino acids R141, Y159, or S163 of Rab27a that disrupt the interaction of Rab27a with Munc13-4, without impairing the interaction between melanophilin and Rab27a.
Whole-exome sequencing reveals overlap between macrophage activation syndrome in systemic juvenile idiopathic arthritis and familial hemophagocytic lymphohistiocytosis.
Grom et al., Cincinnati, United States. In Arthritis Rheumatol, 2014
RESULTS: Heterozygous protein-altering rare variants in the known genes (LYST,MUNC13-4, and STXBP2) were found in 5 of 14 patients with systemic JIA and MAS (35.7%).
Synergistic defects of different molecules in the cytotoxic pathway lead to clinical familial hemophagocytic lymphohistiocytosis.
Filipovich et al., Cincinnati, United States. In Blood, 2014
Several molecules (LYST, AP3, RAB27A, STX11, STXBP2, MUNC13-4, and PRF1) have been associated with the function of cytotoxic lymphocytes.
Contact-induced clustering of syntaxin and munc18 docks secretory granules at the exocytosis site.
Barg et al., Uppsala, Sweden. In Nat Commun, 2013
Here we provide quantitative measurements of several exocytosis proteins (syntaxin, SNAP25, munc18, munc13 and rab3) at the insulin granule release site and show that docking coincides with rapid de novo formation of syntaxin1/munc18 clusters at the nascent docking site.
MUNC13-4 protein regulates the oxidative response and is essential for phagosomal maturation and bacterial killing in neutrophils.
Catz et al., Los Angeles, United States. In J Biol Chem, 2013
MUNC13-4 is a RAB27A effector that coordinates exocytosis in hematopoietic cells, and its deficiency is associated with the human immunodeficiency familial hemophagocytic lymphohistiocytosis type 3.
Munc13 controls the location and efficiency of dense-core vesicle release in neurons.
Toonen et al., Amsterdam, Netherlands. In J Cell Biol, 2013
In munc13-1/2-null mutant neurons, synaptic DCV release was reduced but not abolished, and synaptic preference was lost.
Munc13-independent vesicle priming at mouse photoreceptor ribbon synapses.
Varoqueaux et al., Göttingen, Germany. In J Neurosci, 2012
photoreceptor ribbon synapses and conventional synapses differ fundamentally with regard to their dependence on synaptic vesicles priming proteins of the Munc13 family
[Screening for cytotoxic defects with flow cytometric detection of CD107α on natural killer cells and cytotoxic lymphocyte cells].
Zhao et al., Chongqing, China. In Zhonghua Er Ke Za Zhi, 2012
There was no mutation identified in the LYST gene for patient 2. CD107α expression of NK cells and CTL in the suspected FHL patients and in mirror of these findings, no underlying gene variation of PRF, MUNC13-4 and STX11 were identified.
Munc13-4*rab27 complex tethers secretory lysosomes at the plasma membrane.
van der Sluijs et al., In Commun Integr Biol, 2012
Rab27a and munc13-4 interact directly and are required for target cell killing.
Inhibition of exocytosis or endocytosis blocks activity-dependent redistribution of synapsin.
Daniel et al., Beersheba, Israel. In J Neurochem, 2012
We report that blockage of exocytosis in cultured mouse hippocampal neurons, either by tetanus toxin or by the deletion of munc13, inhibits the activity-dependent redistribution of synapsin from the pre-synaptic terminal into the axon.
Munc13-1 is required for presynaptic long-term potentiation.
Calakos et al., Durham, United States. In J Neurosci, 2011
Disruption of Munc13-1 function inhibits mossy fiber long-term potentiation
RIM proteins activate vesicle priming by reversing autoinhibitory homodimerization of Munc13.
Südhof et al., Stanford, United States. In Neuron, 2011
Data show that homodimerization of Munc13 inhibits its synaptic vesicle priming function, and RIMs activate priming by disrupting Munc13 homodimerization.
Angeborene hämophagozytische Lymphohistiozytose (HLH).
de Saint Basile et al., Zürich, Switzerland. In Klin Padiatr, 2010
Disease-causing mutations in the genes encoding perforin (PRF1, FHL2), munc13-4 (UNC13D, FHL3), syntaxin 11 (STX11, FHL4), and munc18-2 (UNC18-2/STXBP2, FHL5) have been previously identified in Familial Hemophagocyic Lymphohistiocytosis (FHL), whereas mutation in RAB27A and LYST account for Griscelli syndome type 2 and Chediak-Higashi syndrome, respectively.
Munc18 and Munc13 regulate early neurite outgrowth.
Verhage et al., Amsterdam, Netherlands. In Biol Cell, 2010
Munc18, but not Munc13, regulates growth cone filopodia, potentially via its previously observed effect on filamentous actin.
Fbxo45, a novel ubiquitin ligase, regulates synaptic activity.
Okano et al., Tokyo, Japan. In J Biol Chem, 2010
Data suggest that Fbxo45 plays an important role in the regulation of neurotransmission by modulating Munc13-1 at the synapse.
A network of G-protein signaling pathways control neuronal activity in C. elegans.
Nurrish et al., London, United Kingdom. In Adv Genet, 2008
DAG acts via at least two effectors, MUNC13 and PKC, to control the release of both neurotransmitters and neuropeptides from motorneurons.
Review of hemophagocytic lymphohistiocytosis (HLH) in children with focus on Japanese experiences.
Yasukawa et al., Saga, Japan. In Crit Rev Oncol Hematol, 2005
Furthermore, in 2003, MUNC13-4 mutations were identified in some non-FHL2 patients (FHL3).
Regulated exocytosis and SNARE function (Review).
Söllner, New York City, United States. In Mol Membr Biol, 2003
At the neuronal synapse, munc13 as well as munc18 control SNARE complex assembly.
Priming in exocytosis: attaining fusion-competence after vesicle docking.
Martin et al., Madison, United States. In Biochimie, 2000
In addition, munc13 is an important protein involved in priming synaptic vesicles.
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