Analysis of inflammasomes and antiviral sensing components reveals decreased expression of NLRX1 in HIV-positive patients assuming efficient antiretroviral therapy.
Reggio nell'Emilia, Italy. In Aids, Oct 2015
By RT-PCR, using peripheral blood mononuclear cells (PBMCs), we quantified the mRNA expression of 16 genes involved in inflammasome activation and regulation (AIM2, NAIP, PYCARD, CASP1, CASP5, NLRP6, NLRP1, NLRP3, TXNIP, BCL2, NLRC4, PANX1, P2RX7, IL-18, IL-1β, SUGT1) and eight genes involved in IMS (MFN2, MFN1, cGAS, RIG-I, MAVS, NLRX1, RAB32, STING).
Extracellular matrix disruption is an early event in the pathogenesis of skeletal disease in mucopolysaccharidosis I.
Vancouver, Canada. In Mol Genet Metab, Feb 2015
Genome-wide expression studies in embryonic day 13.5 limb cartilage and 5 week growth plate cartilage followed by specific gene candidate qPCR studies in the 5week growth plate identified fourteen significantly deregulated mRNAs (Adamts12, Aspn, Chad, Col2a1, Col9a1, Hapln4, Lum, Matn1, Mmp3, Ogn, Omd, P4ha2, Prelp, and Rab32).
Host restriction in Salmonella: insights from Rab GTPases.
Aberdeen, United Kingdom. In Cell Microbiol, 2014
Recently, an antimicrobial traffic pathway dependent on the Rab GTPase Rab32 and its exchange factor BLOC-3 was found to be critical to kill S. Typhi in macrophages from non-susceptible hosts, suggesting that this pathway delivers an antimicrobial factor to the S. Typhi vacuole.
Regulation of autophagy by the Rab GTPase network.
Chongqing, China. In Cell Death Differ, 2014
Rab1, Rab5, Rab7, Rab9A, Rab11, Rab23, Rab32, and Rab33B participate in autophagosome formation, whereas Rab9 is required in non-canonical autophagy.
A novel anti-microbial function for a familiar Rab GTPase.
New Haven, United States. In Small Gtpases, 2013
We recently reported that a pathway dependent on the Rab GTPase Rab32 and its guanine-nucleotide exchange factor BLOC-3 restricts the growth and survival of S. Typhi in non-permissive macrophages.