The esterase, phosphatase, and sulfatase activities of carbonic anhydrase (CA, EC 4.2.1.1) isozymes, CA I, II, and XIII with 4-nitrophenyl esters as substrates was investigated. These enzymes show esterase activity with 4-nitrophenyl acetate as substrate, with second order rate constants in the range of 753-7706M(-1)s(-1), being less effective as phosphatases (k(cat)/K(M) in the range of 14.89-1374.40M(-1)s(-1)) and totally ineffective sulfatases. The esterase/phosphatase activities were inhibited by sulfonamide CA inhibitors, proving that the zinc-hydroxide mechanism responsible for the CO(2) hydrase activities of CAs is also responsible for their esterase/phosphatase activity. CA XIII was the most effective esterase and phosphatase. CA XIII might catalyze other physiological reactions than CO(2) hydration, based on its relevant phosphatase activity.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.bmcl.2008.03.012DOI Listing

Publication Analysis

Top Keywords

esterase phosphatase
12
phosphatase sulfatase
8
sulfatase activities
8
carbonic anhydrase
8
xiii 4-nitrophenyl
8
4-nitrophenyl esters
8
esters substrates
8
investigations esterase
4
phosphatase
4
activities
4

Similar Publications

The Potential Role of Sanguinarine as an Inhibitor of Leishmania PP2C in the Induction of Apoptosis.

Acta Parasitol

January 2025

División de Investigación, Facultad de Medicina, Unidad de Investigación UNAM-INC, Universidad Nacional Autónoma de México, Instituto Nacional de Cardiología Ignacio Chávez, Juan Badiano No. 1, Col. Sección XVI, Ciudad de México, C.P. 14080, México.

Leishmania spp. cause a wide range of human diseases, localized skin lesions, mucocutaneous and visceral infections. In the present study, the aim was to investigate the potential role of sanguinarine as a specific inhibitor of Leishmania PP2C that can induce apoptosis in the parasite.

View Article and Find Full Text PDF

Unlabelled: Spondyloenchondrodysplasia (SPENCD) is a rare genetic disorder characterized with skeletal dysplasia, immune dysregulation, and neurological impairment. Patients diagnosed with SPENCD at a single pediatric hematology center were included in the study. The patients' clinical characteristics, symptoms at presentation, imaging and laboratory results, and genetic analysis results were collected retrospectively from their files.

View Article and Find Full Text PDF

A fluorescence probe for "switch-on" detection of alkaline phosphatase (ALP) was developed based on Au nanoclusters anchored MnO nanosheets (Au NCs-MnO NSs), which were synthesized using bovine serum albumin (BSA) as template through a simple one-pot approach. In the sensing system, MnO NSs function as both energy acceptors and target identifiers, effectively quenches the fluorescence of Au NCs via fluorescence resonance energy transfer (FRET). The presence of ALP catalyzes the hydrolysis of L-ascorbic acid-2-phosphate (AAP) to ascorbic acid (AA), reducing MnO NSs to Mn and facilitate the fluorescence recovery of Au NCs.

View Article and Find Full Text PDF

Inhibiting Autophagy by Chemicals During SCAPs Osteodifferentiation Elicits Disorganized Mineralization, While the Knock-Out of Genes Leads to Cell Adaptation.

Cells

January 2025

The Laboratory for the Bioengineering of Tissues (BioTis U1026), National Institute of Health and Medical Research (INSERM), Université de Bordeaux, F-33000 Bordeaux, France.

SCAPs (Stem Cells from Apical Papilla), derived from the apex of forming wisdom teeth, extracted from teenagers for orthodontic reasons, belong to the MSCs (Mesenchymal Stromal Cells) family. They have multipotent differentiation capabilities and are a potentially powerful model for investigating strategies of clinical cell therapies. Since autophagy-a regulated self-eating process-was proposed to be essential in osteogenesis, we investigated its involvement in the SCAP model.

View Article and Find Full Text PDF

Chronic Rapamycin Prevents Electrophysiological and Morphological Alterations Produced by Conditional Pten Deletion in Mouse Cortex.

Cells

January 2025

IDDRC, Jane and Terry Semel Institute for Neuroscience and Human Behavior, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA 90095, USA.

Abnormalities in the mammalian target of the rapamycin (mTOR) pathway have been implicated in numerous developmental brain disorders. While the molecular and histological abnormalities have been described, less is known about alterations in membrane and synaptic excitability with chronic changes in the mTOR pathway. In the present study, we used a conditional mouse model with a deletion of the phosphatase and tensin homologue (Pten, a negative regulator of mTOR) from cortical pyramidal neurons (CPNs).

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!