CMV mScarlet-LC3B
By savannah onMammalian expression of fluorescently-tagged marker for autophagic vesicles.
PGK mScarlet-LC3B
By savannah onMammalian expression of fluorescently-tagged marker for autophagic vesicles.
pBMN_HA-TBK1 (kinase dead – D135N)
By savannah onUsed for the expression of TBK1 carrying a kinase dead mutation D135N (SMC Internal No. 1997).
pBMN_HA-TBK1 (E696K)
By savannah onUsed for the expression of TBK1 carrying E696K mutation (SMC Internal No. 1998).
HeLa S3 ATG3 KO
By savannah onHeLa S3 ATG3 KO, CVCL_C7IT Population: African American Knockout cell: Method=CRISPR/Cas9; HGNC; 20962; ATG3 Transformant: NCBI_TaxID; 333761; Human papillomavirus type 18 (HPV18) Miscellaneous: Cell line information from personal communication of Skulsuppaisarn M. Derived from sampling site: Uterus; cervix
Phosphosite mapping on PI3Kc1 by ULK1 and TBK1 kinases (Dataset)
By savannah onThe bands for each subunit of the PI3KC3-C1 complex (VPS15, VPS34, ATG14, and Beclin1) were extracted from the gel and submitted for mass spectrometry analysis.
Unconventional initiation of PINK1/Parkin mitophagy by optineurin
By savannah onThis work reveals that OPTN mitophagy initiation is mechanistically distinct and highlights the mechanistic plasticity of selective autophagy pathways.
shoebridges/asap_phosphosites: Preview release
By savannah onData associated with publication, "Unconventional Initiation of PINK1/Parkin Mitophagy by Optineurin."
Spatial transcriptomics reveals molecular dysfunction associated with Lewy pathology
By savannah onPublished: The results identify neurons vulnerable to Lewy pathology in the PD cortex and identify a conserved signature of molecular dysfunction in both mice and humans. View original preprint.
Post-fibrillization nitration of alpha-synuclein abolishes its seeding activity and pathology formation in primary neurons and in vivo
By savannah onThe pattern of PTMs on pathological aggregates, rather than simply their presence, could be a key determinant of their toxicity and neurodegeneration and reconsidering current approaches relying solely on quantifying and correlating the level of pathology to assess the efficacy of novel therapies, as not all α-Syn aggregates in the brain are pathogenic.
LRRK2 suppresses lysosome degradative activity in macrophages and microglia through MiT-TFE transcription factor inhibition
By savannah onPublished: These discoveries define a mechanism for LRRK2-dependent control of lysosomes and support a model wherein LRRK2 hyperactivity increases Parkinson’s disease risk by suppressing lysosome degradative activity. View original preprint.
Simulations predict differing phase responses to excitation vs. inhibition intheta-resonant pyramidal neurons
By savannah onPublished: The authors hypothesize that intrinsic cellular properties complement network properties and contribute to in vivo phase-shift phenomena such as phase precession, seen in place and grid cells, and phase roll, observed in hippocampal CA1 neurons. View original preprint.
The calcium sensor synaptotagmin-1 is critical for phasic axonal dopamine release in the striatum and mesencephalon, but is dispensable for basic motor behaviors in mice
By savannah onThe authors’ findings reveal the striking resilience of DA-dependent motor functions in the context of a near-abolition of phasic DA release, shedding new light on why extensive loss of DA innervation is required to reveal motor dysfunctions in PD.
Protein aggregation and calcium dysregulation are hallmarks of familial Parkinson’s disease in midbrain dopaminergic neurons
By savannah onOur differentiation paradigm generates an efficient model for studying disease mechanisms in PD and highlights that protein misfolding to generate intraneuronal oligomers is one of the earliest critical events driving disease in human neurons, rather than a late-stage hallmark of the disease.
Parkinson’s VPS35[D620N] mutation induces LRRK2 mediated lysosomal association of RILPL1 and TMEM55B
By savannah onPublished: This study uncovers a pathway through which dysfunctional lysosomes resulting from the VPS35 mutation recruit and activate LRRK2 on the lysosomal surface, driving assembly of the RILPL1-TMEM55B complex. View original preprint.
The lipid flippase ATP10B enables cellular lipid uptake under stress conditions
By savannah onPublished: The authors' data shows that the endo-/lysosomal lipid flippase ATP10B contributes to cellular PC uptake under specific cell stress conditions. View original preprint.
