Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “PROTOZOA”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 847 records · Page 47Linked to original sources
PubMed2001

Calcium in ciliated protozoa: sources, regulation, and calcium-regulated cell functions.

In ciliates, a variety of processes are regulated by Ca2+, e.g., exocytosis, endocytosis, ciliary beat, cell contraction, and nuclear migration. Differential microdomain regulation may occur by activation of specific channels in different cell regions (e.g., voltage-dependent Ca2+ channels in cilia), by local, nonpropagated activation of subplasmalemmal Ca stores (alveolar sacs), by different sensitivity thresholds, and eventually by interplay with additional second messengers (cilia). During stimulus-secretion coupling, Ca2+ as the only known second messenger operates at approximately 5 microM, whereby mobilization from alveolar sacs is superimposed by "store-operated Ca2+ influx" (SOC), to drive exocytotic and endocytotic membrane fusion. (Content discharge requires binding of extracellular Ca2+ to some secretory proteins.) Ca2+ homeostasis is reestablished by binding to cytosolic Ca2+-binding proteins (e.g., calmodulin), by sequestration into mitochondria (perhaps by Ca2+ uniporter) and into endoplasmic reticulum and alveolar sacs (with a SERCA-type pump), and by extrusion via a plasmalemmal Ca2+ pump and a Na+/Ca2+ exchanger. Comparison of free vs total concentration, [Ca2+] vs [Ca], during activation, using time-resolved fluorochrome analysis and X-ray microanalysis, respectively, reveals that altogether activation requires a calcium flux that is orders of magnitude larger than that expected from the [Ca2+] actually required for local activation.

Animals↗
PubMedDate not supplied

Antimicrobial and cytolytic polypeptides of amoeboid protozoa--effector molecules of primitive phagocytes.

Amoebae are primitive, actively phagocytosing eukaryotic cells, many of which use bacteria as a major nutrient source. One may suppose that amoebae possess an array of potent antimicrobial molecules acting in synergy to combat bacterial growth inside their phagosomes. Lysosome-like granular vesicles of Entamoeba histolytica contain a family of 77-residue peptides with a compact alpha-helical, disulfide-bonded fold. These polypeptides, named amoebapores, exhibit antibacterial and cytolytic activity by forming pores in membranes of various origin. It is of particular interest that amoebapores are structurally and functionally most similar to polypeptides of mammalian cytotoxic lymphocytes. In addition, amoebic granules contain bacteriolytic proteins with lysozyme-like properties. Some amoebic polypeptides may represent archaic analogs of effector molecules from invertebrates and vertebrates.

Amino Acid Sequence↗
PubMed2003

Fatty acid and sterol metabolism: potential antimicrobial targets in apicomplexan and trypanosomatid parasitic protozoa.

Current treatments for diseases caused by apicomplexan and trypanosomatid parasites are inadequate due to toxicity, the development of drug resistance and an inability to eliminate all life cycle stages of these parasites from the host. New therapeutics agents are urgently required. It has recently been demonstrated that type II fatty acid biosynthesis occurs in the plastid of Plasmodium falciparum and Toxoplasma gondii and inhibitors of this pathway such as triclosan and thiolactomycin restrict their growth. Furthermore, Trypanosoma brucei has recently been demonstrated to use type II fatty acid biosynthesis for myristate synthesis and to be susceptible to thiolactomycin. As this pathway is absent from mammals, it may provide an excellent target for novel antimicrobial agents to combat these diverse parasites. Leishmania and Trypanosoma parasites produce ergosterol-related sterols by a biosynthetic pathway similar to that operating in pathogenic fungi and their growth is susceptible to sterol biosynthesis inhibitors. Thus, inhibition of squalene 2,3-epoxidase by terbinafine, 14alpha-methylsterol 14-demethylase by azole and triazole compounds and delta(24)-sterol methyl transferase by azasterols all cause a depletion of normal sterols and an accumulation of abnormal amounts of sterol precursors with cytostatic or cytoxic consequences. However, Leishmania parasites can survive with greatly altered sterol profiles induced by continuous treatment with low concentrations of some inhibitors and they also have some ability to utilise and metabolise host sterol. These properties may permit the parasites to evade treatment with sterol biosynthesis inhibitors in some clinical situations and need to be taken into account in the design of future drugs.

Animals↗
PubMed1997

The genomic organization of guide RNA genes in kinetoplastid protozoa: several conundrums and their solutions.

The guide RNA (gRNA) paradigm states that the uridine (U) insertion/deletion type of RNA editing is mediated by short 3' uridylylated gRNAs that are complementary to specific blocks of mature edited sequence. These gRNAs contain the edited sequence information in the form of guiding purine residues that can base pair with the inserted U's and do not base pair with encoded U's that are to be deleted. The minicircle gRNA genes in trypanosomatids are localized at specific sites within the variable region, with the number and the precise localization of genes also being species-specific. The total number of minicircle sequence classes and thereby minicircle-encoded gRNAs varies greatly between species and even between different strains of the same species, with the greatest number being in the trypanosome species. Several conundrums which appeared to raise problems for the gRNA paradigm arose during comparative analysis of minicircle gRNA gene organization. The solution of these conundrums has led to a better understanding of the function and evolution of this RNA modification phenomenon.

Animals↗