PMCC PMCC

Search tips
Search criteria

Advanced
Results 1-11 (11)
 

Clipboard (0)
None
Journals
Authors
more »
Year of Publication
Document Types
1.  Unveiling ubiquitinome rearrangements induced by Salmonella infection 
Autophagy  2016;12(9):1683-1684.
ABSTRACT
Ubiquitination plays a critical role in the activation of host immune responses to infection and serves as a signal for pathogen delivery to phagophores along the xenophagy pathway. We recently performed systematic ubiquitination site profiling of epithelial cells infected with Salmonella Typhimurium. Our findings specifically highlight components of the NFKB, membrane trafficking pathways and RHO GTPase systems as ubiquitination hubs during infection. In addition, a broad spectrum of bacterial effectors and several outer membrane proteins are ubiquitinated in infected cells. This comprehensive resource of ubiquitinome dynamics during Salmonella infection enables further understanding of the complex host-pathogen interplay and may reveal novel targets for the inhibition of Salmonella invasion and inflammation.
doi:10.1080/15548627.2016.1203490
PMCID: PMC5082772  PMID: 27467224
immune response; Salmonella infection; ubiquitin coat; ubiquitination; xenophagy
4.  The ABC of Ribosome-Related Antibiotic Resistance 
mBio  2016;7(3):e00598-16.
ABSTRACT
The increase in multidrug-resistant pathogenic bacteria is limiting the utility of our current arsenal of antimicrobial agents. Mechanistically understanding how bacteria obtain antibiotic resistance is a critical first step to the development of improved inhibitors. One common mechanism for bacteria to obtain antibiotic resistance is by employing ATP-binding cassette (ABC) transporters to actively pump the drug from the cell. The ABC-F family includes proteins conferring resistance to a variety of clinically important ribosome-targeting antibiotics; however, controversy remains as to whether resistance is conferred via efflux like other ABC transporters or whether another mechanism, such as ribosome protection, is at play. A recent study by Sharkey and coworkers (L. K. Sharkey, T. A. Edwards, and A. J. O’Neill, mBio 7:e01975-15, 2016, http://dx.doi.org/10.1128/mBio.01975-15) provides strong evidence that ABC-F proteins conferring antibiotic resistance utilize ribosome protection mechanisms, namely, by interacting with the ribosome and displacing the drug from its binding site, thus revealing a novel role for ABC-F proteins in antibiotic resistance.
doi:10.1128/mBio.00598-16
PMCID: PMC4959660  PMID: 27143393
5.  Possible regulation of caveolar endocytosis and flattening by phosphorylation of F-BAR domain protein PACSIN2/Syndapin II  
Bioarchitecture  2016;5(5-6):70-77.
ABSTRACT. Caveolae are flask-shaped invaginations of the plasma membrane. The BAR domain proteins form crescent-shaped dimers, and their oligomeric filaments are considered to form spirals at the necks of invaginations, such as clathrin-coated pits and caveolae. PACSIN2/Syndapin II is one of the BAR domain-containing proteins, and is localized at the necks of caveolae. PACSIN2 is thought to function in the scission and stabilization of caveolae, through binding to dynamin-2 and EHD2, respectively. These two functions are considered to be switched by PACSIN2 phosphorylation by protein kinase C (PKC) upon hypotonic stress and sheer stress. The phosphorylation decreases the membrane binding affinity of PACSIN2, leading to its removal from caveolae. The removal of the putative oligomeric spiral of PACSIN2 from caveolar membrane invaginations could lead to the deformation of caveolae. Indeed, PACSIN2 removal from caveolae is accompanied by the recruitment of dynamin-2, suggesting that the removal provides space for the function of dynamin-2. Otherwise, the removal of PACSIN2 decreases the stability of caveolae, which could result in the flattening of caveolae. In contrast, an increase in the amount of EHD2 restored caveolar stability. Therefore, PACSIN2 at caveolae stabilizes caveolae, but its removal by phosphorylation could induce both caveolar endocytosis and flattening.
doi:10.1080/19490992.2015.1128604
PMCID: PMC4832444  PMID: 26745030
BAR domain; caveolae; mechanical stress; phosphorylation; protein kinase C
6.  Leukocyte adhesion and polarization: Role of glycosylphosphatidylinositol-anchored proteins 
Bioarchitecture  2016;5(5-6):61-69.
ABSTRACT
Leukocyte traffic out of the blood stream is crucial for an adequate immune response. Leukocyte extravasation is critically dependent on the binding of leukocyte integrins to their endothelial counterreceptors. This interaction enables the firm adhesion of leukocytes to the luminal side of the vascular wall and allows for leukocyte polarization, crawling and diapedesis. Leukocyte adhesion, polarization and migration requires the orchestrated regulation of integrin adhesion/de-adhesion dynamics and actin cytoskeleton rearrangements. Adhesion strength depends on conformational changes of integrin molecules (affinity) as well as the number of integrin molecules engaged at adhesion sites (valency). These two processes can be independently regulated and several molecules modulate either one or both processes. Cholesterol-rich membrane domains (lipid rafts) participate in integrin regulation and play an important role in leukocyte adhesion, polarization and motility. In particular, lipid raft-resident glycosyl-phosphatidyl-inositol-anchored proteins (GPI-APs) have been reported to regulate leukocyte adhesion, polarization and motility in both integrin-dependent and independent manners. Here, we present our recent discovery concerning the novel role of the GPI-AP prion protein (PrP) in the regulation of β1 integrin-mediated monocyte adhesion, migration and shape polarization in the context of existing literature on GPI-AP-dependent regulation of integrins.
doi:10.1080/19490992.2015.1127466
PMCID: PMC4832445  PMID: 26744925
GPI-anchored protein; lipid raft; ERM; leukocyte; integrin; uropod; polarization; migration; diapedesis
7.  A clarion call or a swan song? Commentary: A crisis in comparative psychology: where have all the undergraduates gone? 
Frontiers in Psychology  2015;6:1867.
doi:10.3389/fpsyg.2015.01867
PMCID: PMC4667089  PMID: 26696933
comparative psychology; animal behavior; comparative cognition; evolutionary psychology; ethology
8.  It's just evolution. Commentary: A crisis in comparative psychology: where have all the undergraduates gone? 
Frontiers in Psychology  2015;6:1873.
doi:10.3389/fpsyg.2015.01873
PMCID: PMC4667097  PMID: 26696937
comparative psychology; evolution; undergraduate students; cognition; recruitment; comparative cognition
9.  Comments on Statistical Issues in September 2015 
Korean Journal of Family Medicine  2015;36(5):258-259.
doi:10.4082/kjfm.2015.36.5.258
PMCID: PMC4591393  PMID: 26435818
10.  Eye-of-the-Tiger sign is not Pathognomonic of Pantothenate Kinase-Associated Neurodegeneration in Adult Cases 
Brain and Behavior  2011;1(1):55-56.
An eye-of-the-tiger sign is previously known to have one-to-one correlation with pantothenate kinase-associated neurodegeneration (PKAN). Reviewing the literature on this subject, the correlation between eye-of-the-tiger sign and PKAN seems to show an interesting hypothesis that differs from conventional conclusion. We analyze the published papers in an attempt to reflect this trend and illustrate our points with findings in a 39-year-old man. His brain magnetic resonance imaging study shows typical eye-of-the-tiger sign suggestive of PKAN. Genetic analyses revealed no mutations in pantothenate kinase 2.
doi:10.1002/brb3.8
PMCID: PMC3217674  PMID: 22398981
Neurodegeneration with brain iron accumulation; pantothenate kinase-associated neurodegeneration; pantothenate kinase 2; eye-of-the-tiger sign; PKAN; NBIA; Hallervorden-Spatz syndrome
11.  Challenges in diagnosis of isolated central nervous system vasculitis 
Brain and Behavior  2011;1(1):57-61.
Isolated central nervous system (CNS) vasculitis is a rare and complicated disorder. Patients typically present with nonspecific neurologic symptoms such as headache and encephalopathy, and have variable progression and severity of the disease. Challenges to definitive diagnosis include the limitations of currently available diagnostic modalities with high likelihood of false-positive or false-negative findings. Imaging, serologic, and cerebrospinal fluid (CSF) evaluation, and even angiography can fail to establish the diagnosis. Often, brain biopsy is required. In order to illustrate these challenges, we report the case of a patient who presented with subacute cognitive decline and was ultimately diagnosed with isolated CNS eosinophilic vasculitis. Initial work-up included CSF and serologic analyses, magnetic resonance imaging (MRI), and cerebral angiography, but definitive diagnosis required brain biopsy. Immunosuppressive therapy resulted in clinical improvement and stabilization. To our knowledge, only one other case of isolated CNS eosinophilic vasculitis has been reported in the literature. We discuss the importance of a high index of clinical suspicion in cases of progressive nonspecific neurologic symptoms.
doi:10.1002/brb3.12
PMCID: PMC3217675  PMID: 22398982
Vasculitis; hypereosinophilic syndrome; primary angiitis of the central nervous system; memory; aphasia

Results 1-11 (11)