Loss of Bardet-Biedl syndrome proteins causes synaptic aberrations in principal neurons

scientific article published on 03 September 2019

Loss of Bardet-Biedl syndrome proteins causes synaptic aberrations in principal neurons is …
instance of (P31):
scholarly articleQ13442814

External links are
P356DOI10.1371/JOURNAL.PBIO.3000414
P932PMC publication ID6743795
P698PubMed publication ID31479441

P50authorMichael HausserQ19926268
Patricia C SalinasQ55966247
Janosch P D HellerQ56419973
S. WellsQ67390418
Michael C WuQ93073888
Christoph Schmidt-HieberQ38322688
Richard J RodenburgQ41825611
Fernando J SialanaQ50275424
P2093author name stringPhilip L Beales
Michelle Stewart
Gert Lubec
Lorenza Ciani
Liz Bentley
Elizabeth Forsythe
Patrick M Nolan
Naila Haq
Sofia Christou-Savina
P2860cites workBasal body dysfunction is a likely cause of pleiotropic Bardet-Biedl syndromeQ24296493
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The Cdc42 effector IRSp53 generates filopodia by coupling membrane protrusion with actin dynamicsQ24336730
The Bardet-Biedl protein BBS4 targets cargo to the pericentriolar region and is required for microtubule anchoring and cell cycle progressionQ24337908
Clinical and genetic epidemiology of Bardet-Biedl syndrome in Newfoundland: a 22-year prospective, population-based, cohort studyQ24622509
Reactive oxygen species are essential for autophagy and specifically regulate the activity of Atg4Q24670840
Loss of Bardet Biedl syndrome proteins causes defects in peripheral sensory innervation and functionQ24678735
New criteria for improved diagnosis of Bardet-Biedl syndrome: results of a population surveyQ24681777
Structural plasticity of dendritic spinesQ27002957
Biochemical diagnosis of mitochondrial disordersQ27990527
The insulin receptor tyrosine kinase substrate p58/53 and the insulin receptor are components of CNS synapsesQ28142887
WAVE2 serves a functional partner of IRSp53 by regulating its interaction with RacQ28203310
Loss of mTOR-dependent macroautophagy causes autistic-like synaptic pruning deficitsQ28246677
Dendritic Spine Instability in a Mouse Model of CDKL5 Disorder Is Rescued by Insulin-like Growth Factor 1Q28268294
Disruption of Bardet-Biedl syndrome ciliary proteins perturbs planar cell polarity in vertebratesQ28506652
Bardet-Biedl syndrome proteins are required for the localization of G protein-coupled receptors to primary ciliaQ28506905
Arl13b-regulated cilia activities are essential for polarized radial glial scaffold formationQ28507617
Bardet-Biedl syndrome proteins control the cilia length through regulation of actin polymerizationQ28511839
Primary cilia regulate proliferation of amplifying progenitors in adult hippocampus: implications for learning and memoryQ28590555
Loss of BBS proteins causes anosmia in humans and defects in olfactory cilia structure and function in the mouseQ28593460
Restoration of physiological expression of 5-HT6 into the primary cilia of null mutant neurons lengthens both primary cilia and dendrites.Q52313842
Proteomic Studies on the Swim Bladder of the European Eel (Anguilla anguilla).Q54244034
EphB maintains dendritic spine morphology through focal adhesion kinase.Q54713964
Quantal components of unitary EPSCs at the mossy fibre synapse on CA3 pyramidal cells of rat hippocampusQ72673164
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Basal body proteins regulate Notch signaling through endosomal traffickingQ33687596
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The role of Insulin-Like Growth Factor 1 (IGF-1) in brain development, maturation and neuroplasticityQ38796469
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Interaction between interferon gamma and insulin-like growth factor-1 in hippocampus impacts on the ability of rats to sustain long-term potentiationQ48658293
Quantitative Proteomics of Synaptosomal Fractions in a Rat Overexpressing Human DISC1 Gene Indicates Profound Synaptic Dysregulation in the Dorsal StriatumQ50275244
P275copyright licenseCreative Commons Attribution 4.0 InternationalQ20007257
P6216copyright statuscopyrightedQ50423863
P4510describes a project that usesImageJQ1659584
P433issue9
P921main subjectBardet-Biedl syndromeQ1678281
P304page(s)e3000414
P577publication date2019-09-03
P1433published inPLOS BiologyQ1771695
P1476titleLoss of Bardet-Biedl syndrome proteins causes synaptic aberrations in principal neurons
P478volume17

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cites work (P2860)
Q90589879Correction: Loss of Bardet-Biedl syndrome proteins causes synaptic aberrations in principal neurons
Q95319070The absence of BBSome function decreases synaptogenesis and causes ectopic synapse formation in the retina

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