Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:3.4.24.11 (
CD10
)
9,792
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Alzheimer's disease is a progressive brain disorder with the loss of memory and other intellectual abilities. Amyloid species and neurofibrillary tangles are the prime suspects in damaging and killing nerve cells. Abnormal accumulation of Amyloid-beta peptide (Abeta) may cause synaptic dysfunction and degeneration of neurons. Drugs that can prevent its formation and accumulation or stimulate its clearance might ultimately be of therapeutic benefit. Ciliary neurotrophic factor (CNTF), a neurotrophic cytokine, promotes the survival of various neurons in brain. However, the blood-brain barrier hinders the systemic delivery of CNTF to brain. Recently the 11-amino acid of protein transduction domain
TAT
has successfully assisted the delivery of many macromolecules to treat preclinical models of human disease. The present study aimed to evaluate whether P11-CNTF fusion protein (P11-CNTF) is protective against the Abeta25-35-induced dementia in mice. Immunofluorescence experiments showed that P11 effectively carried CNTF to the SH-SY5Y cells in vitro, and to the brains of mice in vivo. The learning and memory impairments of mice induced by Abeta were substantially rescued by supplement with the P11-CNTF. Furthermore, mRNAs of enzymes involved in the Abeta metabolism, e.g.
neprilysin
(
NEP
), endothelin-converting enzyme 1 (ECE-1) and insulin degrading enzyme (IDE), increased in the P11-CNTF treated dementia mice, accompanied by the proliferation of nestin- and choline acetyltransferase (ChAT)-positive cells in hippocampus. It implies that the delivery of P11-CNTF may be a novel treatment for Alzheimer's disease.
...
PMID:Transducible P11-CNTF rescues the learning and memory impairments induced by amyloid-beta peptide in mice. 1864 61
The diffusion of KPC-2 carbapenemase is closely related to the spread of
Klebsiella pneumoniae
of the clonal-group 258 and linked to IncFII
K
plasmids. Little is known about the biology of multi-drug resistant plasmids and the reasons of their successful dissemination. Using
E. coli
TOP10 strain harboring a multi-replicon IncFII
K
-IncFIB
bla
KPC-2
-gene carrying plasmid pBIC1a from
K. pneumoniae
ST-258 clinical isolate BIC-1, we aimed to identify basal gene expression and the effects of imipenem exposure using whole transcriptome approach by RNA sequencing (RNA-Seq). Independently of the antibiotic pressure, most of the plasmid-backbone genes were expressed at low levels. The most expressed pBIC1a genes were involved in antibiotic resistance (
bla
KPC-2
,
bla
TEM
and
aph
(3')-I), in plasmid replication and conjugation, or associated to mobile elements. After antibiotic exposure, 34% of
E. coli
(pBIC1a) genome was differentially expressed. Induction of oxidative stress response was evidenced, with numerous upregulated genes of the
SoxRS/OxyR
oxydative stress regulons, the Fur regulon (for iron uptake machinery), and
IscR
regulon (for iron sulfur cluster synthesis). Nine genes carried by pBIC1a were up-regulated, including the murein DD-
endopeptidase
mepM
and the copper resistance operon. Despite the presence of a carbapenemase, we observed a major impact on
E. coli
(pBIC1a) whole transcriptome after imipenem exposure, but no effect on the level of transcription of antimicrobial resistance genes. We describe adaptive responses of
E. coli
to imipenem-induced stress, and identified plasmid-encoded genes that could be involved in resistance to stressful environments.
...
PMID:Transcriptional Landscape of a
bla
KPC-2
Plasmid and Response to Imipenem Exposure in
Escherichia coli
TOP10. 3055 31
