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| 1 | Dying by fire: noncanonical functions of autophagy proteins in neuroinflammation and neurodegeneration显示文摘Neuroinflammation and neurodegeneration are key components in the establishment and progression of neurodegenerative diseases including Alzheimer's Disease(AD). Over the past decade increasing evidence is emerging for the use of components of the canonical autophagy machinery in pathways that are characterized by LC3 lipidation yet are distinct from traditional macro-autophagy. One such pathway that utilizes components of the autophagy machinery to target LC3 to endosomes, a process termed LC3-associated endocytosis(LANDO), has recently been identified and regulates neuroinflammation. Abrogation of LANDO in microglia cells results in a propensity for elevated neuroinflammatory cytokine production. Using the well-established 5 xFAD model of AD to interrogate neuroinflammatory regulation, impairment of LANDO through deletion of a key upstream regulator Rubicon or other downstream autophagy components, exacerbated disease onset and severity, while deletion of microglial autophagy alone had no measurable effect. Mice presented with robust deposition of the neurotoxic AD protein β-amyloid(Aβ), microglial activation and inflammatory cytokine production, tau phosphorylation, and aggressive neurodegeneration culminating in severe memory impairment. LANDO-deficiency impaired recycling of receptors that recognize Aβ, including TLR4 and TREM2. LANDO-deficiency alone through deletion of the WD-domain of the autophagy protein ATG16 L, revealed a role for LANDO in the spontaneous establishment of age-associated AD. LANDO-deficient mice aged to 2 years presented with advanced ADlike disease and pathology correlative to that observed in human AD patients. Together, these studies illustrate an important role for microglial LANDO in regulating CNS immune activation and protection against neurodegeneration. New evidence is emerging that demonstrates a putative linkage between pathways such as LANDO and cell death regulation via apoptosis and possibly necroptosis. Herein, we provide a review of the use of the autophagy machinery in non-canonical mechanisms that alter immune regulation and could have significant impact in furthering our understanding of not only CNS diseases like AD, but likely beyond. | Alexis D.Rickman Addison Hilyard Bradlee L.Heckmann | 2022 | Neural Regeneration Research2022，17，2： | 3 |
| 2 | Molecular basis for antagonism between PDGF and the TGFbeta family of signalling pathways by control of miR-24 expression显示文摘 | Chan MC Hilyard AC Wu C | 2010 | EMBO J2010，29，： | 1 |
| 3 | Bartonella clarridgeiae, a newly recognized zoonotic pathogen causing inoculation papules, fever, and lymphadenopathy (cat scratch disease)显示文摘 | Kordick D L Hilyard E J Hadfield T L | 1997 | J Clin Microbiol1997，35，7： | 1 |
| 4 | SMAD proteins control DROSHA-mediated microRNA maturation 显示文摘 | Davis BN Hilyard AC Lagna G | 2008 | Nature2008，454，7200： | 1 |
| 5 | Bacillus piliformis infection confirmation with 16s ribosomal RNA sequence analysis 显示文摘 | Smith KJ Skelton HG Hilyard in a patient infected with HIV-1 EJ | 1996 | J Am Acad Dermatol1996，34，： | 1 |
| 6 | Blog functions as risk and crisis communication during Hurricane Katrina 显示文摘 | Macias W Hilyard K Freimuth V | 2009 | Journal of Computer-Mediated Communication2009，，15： | 1 |
| 7 | SMAD proteins control DROSHA-mediated microR-NA maturation 显示文摘 | DAVIS B N HILYARD A C LAGNA G | 2008 | Nature2008，454，7200： | 1 |
| 8 | SMAD proteins control DROSHA-mediated microRNA maturation显示文摘 | Davis B N Hilyard A C Lagna G | 2008 | Nature2008，454，7200： | 1 |
| 9 | SMAD proteins control DROSHA-mediated microRNA maturation显示文摘 | Davis BN Hilyard AC Lagna G | | 0，，7200： | 1 |
| 10 | Bacillus piliformis infection (Tyzzer' s disease ) in a patient infected with HIV-1 confirmation with 16S ribosomal RNA sequence analysis显示文摘 | Smith KJ Skehon HG Hilyard EJ | 1996 | J Am Acad Dermatol1996，34，： | 1 |
| 11 | SMAD proteins control DROSHA-me- diated microRNA maturation显示文摘 | Davis BN Hilyard AC Lagna G | 2008 | Nature2008，454，7200： | 1 |
| 12 | Induction of microRNA-221 by platelet-derived growth factor signaling is critical for modulation of vascular smooth muscle phenotype显示文摘 | Davis BN Hilyard AC Nguyen PH | | 0，，06： | 1 |
| 13 | SMAD proteins control DROSHA-mediated microRNA maturation 显示文摘 | Davis B N Hilyard A C Lagna G | 2008 | Nature2008，454，7200： | 1 |
| 14 | Bacillus piliformis infection(Tyzzer's disease)in a patient infected with HIVl:confirmation with 16S ribosomal RNA sequence analysis显示文摘 | Smith KJ Skelton HG Hilyard EJ | 1996 | J Am Acad Dermatol1996，34，： | 1 |
| 15 | Molecular basis for antag- onism between PDGF and the TGFbeta family of signalling path- ways by eontrol of miR-24 expression显示文摘 | Chan M C Hilyard A C Wu C | 2010 | Embo J2010，29，3： | 1 |
| 16 | Molecular basis for antagonism between PDGF and the TGFbeta family of signalling pathways by control of miR-24 expression显示文摘 | Chan MC Hilyard AC Wu C | 2010 | EMBO J2010，29，3： | 1 |
| 17 | Induction of microRNA-221 by platelet derived growth factor signaling is critical for modulation of vascular smooth muscle phenotype 显示文摘 | Davis BN Hilyard AC Nguyen PH | 2009 | J BiolChem2009，284，6： | 1 |
| 18 | Blog functions as risk and crisis communication during Hurricane Katrina 显示文摘 | Marcias W Hilyard K Freimuth V | 2009 | Journal of Computer-Mediated Communication2009，15，1： | 1 |
| 19 | Induction of mi- croRNA-221 by platelet-derived growth factor signaling is critical for modulation of vascular smooth muscle phenotype 显示文摘 | Davis B N Hilyard A C Nguyen P H | 2009 | J Biol Chem2009，284，6： | 1 |
| 20 | IL-12 selectively regulates STAT4 via phosphatidylinositol 3-kinase and Ras-independent signal transduction pathways 显示文摘 | Flotow H Hilyard KL | 2000 | Eur J Immunol2000，30，： | 1 |
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