scholarly journals Metal-replacement studies in Bacillus stearothermophilus aldolase and a comparison of the mechanisms of class I and class II aldolases

1976 ◽  
Vol 153 (3) ◽  
pp. 551-560 ◽  
Author(s):  
H A O Hill ◽  
R R Lobb ◽  
S L Sharp ◽  
A M Stokes ◽  
J I Harris ◽  
...  
Keyword(s):  
Thermal Stability ◽  
Bacillus Stearothermophilus ◽  
Class Ii ◽  
Product Inhibition ◽  
Class I ◽  
Dihydroxyacetone Phosphate ◽  
Rabbit Muscle ◽  
Reaction Sequence ◽  
Cleavage Activity

A comparison of the product-inhibition patterns during cleavage of D-fructose 1,6-diphosphate by aldolases from yeast, rabbit muscle and Bacillus stearothermophilus shows an ordered reaction sequence for all three enzymes, with dihydroxyacetone phosphate the last-leaving product. Addition of Zn2+, Co2+, Fe2+, Mn2+ or Cd2+ ions to the inactive apo-(Bacillus stearothermophilus aldolase) restores activity to different extents, whereas Ni2+, Mg2+ or Cu2+ ions have no effect. The cleavage activity of this aldolase is not enhanced by added K+ ion. The effects of metal replacement on thermal stability, Km and Vmax. are given and the possible role of the metal is discussed in the light of these results.

KINETIC STUDIES ON THE MECHANISM OF CYTOPLASMIC L-α-GLYCEROPHOSPHATE DEHYDROGENASE OF RABBIT SKELETAL MUSCLE

1966 ◽  
Vol 44 (10) ◽  
pp. 1301-1317 ◽  
Author(s):  
William J. Black
Keyword(s):  
Kinetic Data ◽  
Substrate Inhibition ◽  
Product Inhibition ◽  
Reduced Form ◽  
Ultraviolet Absorption Spectrum ◽  
Dihydroxyacetone Phosphate ◽  
Enzyme Complex ◽  
Rabbit Muscle ◽  
Glycerophosphate Dehydrogenase ◽  
Dead End

Studies on initial velocity and product inhibition were carried out on crystalline cytoplasmic NAD+-linked L-α-glycerophosphate dehydrogenase from rabbit muscle, at pH 7.8 and 9.0 at 26 °C. Michaelis and inhibition constants for all the reactants were determined. The kinetic data were consistent with an ordered mechanism in which nicotinamide–adenine dinucleotide (NAD+) or its reduced form (NADH) is bound to the enzyme before the addition of the glycerophosphate (LαGP) or dihydroxyacetone phosphate (DHAP) respectively. At high concentrations NADH, DHAP, and LαGP, but not NAD+, produced substrate inhibition. Combined product-inhibition and dead-end inhibition studies indicated the formation of inactive dead-end complexes of NADH–enzyme, DHAP–enzyme, and LαGP–enzyme–NADH. The low rate constant calculated for the dissociation of the active NADH–enzyme complex suggested an ordered mechanism involving either the formation of an inactive dead-end NADH–enzyme complex or an isomerized NADH–enzyme complex. A choice between these possibilities could not be made on the basis of the present kinetic data. A mechanism for substrate inhibition involving two NAD+-binding sites per mole of enzyme is proposed. Alterations of the ultraviolet absorption spectrum of the enzyme by NAD+ and NADH were in agreement with the conclusion from the kinetic results that the coenzymes are bound to the enzyme before the substrates. DHAP and LαGP caused no alteration in the enzyme spectrum. Spectral changes compatible with the formation of ternary and dead-end complexes were also detected.

scholarly journals Epigenetic regulation of translation repression in ferroptosis, and a role of Alternative splicing and tRNA methylation.

2021 ◽  
Author(s):  
Sherif Rashad ◽  
Daisuke Saigusa ◽  
Yuan Zhou ◽  
Liyin Zhang ◽  
Teiji Tominaga ◽  
...  
Keyword(s):  
Alternative Splicing ◽  
Glioma Cells ◽  
Mrna Translation ◽  
Class Ii ◽  
Class I ◽  
Sequencing Analysis ◽  
Translation Repression ◽  
Transsulfuration Pathway ◽  
The Impact

Ferroptosis is a non-apoptotic cell death mechanism characterized by the production of lipid peroxides. Ferroptosis plays important roles in many diseases such as cancer and neurodegenerative diseases. While many effectors in the ferroptosis pathway have been mapped, its epigenetic and epitranscriptional regulatory processes are not yet fully understood. Ferroptosis can be induced via system xCT inhibition (Class I) or GPX4 inhibition (Class II). Previous works have revealed important differences in cellular response to Class I and Class II ferroptosis inducers. Importantly, blocking mRNA transcription or translation appears to protect cells against Class I ferroptosis inducing agents but not Class II. Understanding these subtle differences is important in understanding ferroptosis as well as in developing therapeutics based on ferroptosis for various diseases. In this work, we examined the impact of blocking transcription (via Actinomycin D) or translation (via Cycloheximide) on Erastin (Class I) or RSL3 (Class II) induced ferroptosis. Blocking transcription or translation protected cells against Erastin but was detrimental against RSL3. Cycloheximide led to increased levels of GSH alone or when co-treated with Erastin and the activation of the reverse transsulfuration pathway. RNA sequencing analysis revealed an important and unexplored role of Alternative splicing (AS) in regulating ferroptosis stress response and mRNA translation repression. Our results indicated that translation repression is protective against Erastin but detrimental against RSL3. We tested this theory in Alkbh1 overexpressing glioma cells. Alkbh1 demethylates tRNA and represses translation and is associated with worse outcome in glioma patients. Our results showed that Alkbh1 overexpression protected glioma cells against Erastin but was detrimental against RSL3.

scholarly journals Contribution of σ70 and σN Factors to Expression of Class II pilE in Neisseria meningitidis

2019 ◽  
Vol 201 (20) ◽  
Author(s):  
Mariya Lobanovska ◽  
Christoph M. Tang ◽  
Rachel M. Exley
Keyword(s):  
Neisseria Meningitidis ◽  
Antigenic Variation ◽  
Cell Interaction ◽  
Class Ii ◽  
Class I ◽  
Epidemic Disease ◽  
Content Type ◽  
Main Component ◽  
Host Cell Interaction

ABSTRACT Neisseria meningitidis expresses multicomponent organelles called type four pili (Tfp), which are key virulence factors required for attachment to human cells during carriage and disease. Pilin (PilE) is the main component of Tfp, and N. meningitidis isolates either have a class I pilE locus and express pilins that undergo antigenic variation or have a class II pilE locus and express invariant pilins. The transcriptional regulation of class I pilE has been studied in both N. meningitidis and Neisseria gonorrhoeae, while the control of expression of class II pilE has been elucidated in the nonpathogenic species Neisseria elongata. However, the factors that govern the regulation of the class II pilE gene in N. meningitidis are not known. In this work, we have bioinformatically and experimentally identified the class II pilE promoter. We confirmed the presence of conserved σ70 and σN-dependent promoters upstream of pilE in a collection of meningococcal genomes and demonstrated that class II pilE expression initiates from the σ70 family-dependent promoter. By deletion or overexpression of sigma factors, we showed that σN, σH, and σE do not affect class II pilin expression. These findings are consistent with a role of the housekeeping σD in expression of this important component of Tfp. Taken together, our data indicate that the σ-dependent network responsible for the expression of class II pilE has been selected to maintain pilE expression, consistent with the essential roles of Tfp in colonization and pathogenesis. IMPORTANCE The type four pilus (Tfp) of Neisseria meningitidis contributes to fundamental processes such as adhesion, transformation, and disease pathology. Meningococci express one of two distinct classes of Tfp (class I or class II), which can be distinguished antigenically or by the major subunit (pilE) locus and its genetic context. The factors that govern transcription of the class II pilE gene are not known, even though it is present in isolates that cause epidemic disease. Here we show that the transcription of class II pilE is maintained throughout growth and under different stress conditions and is driven by a σ70-dependent promoter. This is distinct from Tfp regulation in nonpathogenic Neisseria spp. and may confer an advantage during host-cell interaction and infection.

scholarly journals The role of class I and class II HLA antigens in primary open angle glaucoma (POAG)

2009 ◽  
Vol 76 (S227) ◽  
pp. 17-19
Author(s):  
G. Ferreri ◽  
A. D'Andrea ◽  
I. Castagna ◽  
C. Rechichi ◽  
G. Pettinato ◽  
...  
Keyword(s):  
Primary Open Angle Glaucoma ◽  
Open Angle Glaucoma ◽  
Hla Antigens ◽  
Class Ii ◽  
Class I ◽  
Open Angle

Murine T Lymphocytes Incapable of Producing Macrophage Inhibitory Protein-1 Are Impaired in Causing Graft-Versus-Host Disease Across a Class I But Not Class II Major Histocompatibility Complex Barrier

Blood ◽  
1999 ◽  
Vol 93 (1) ◽  
pp. 43-50 ◽  
Author(s):  
Jonathan S. Serody ◽  
Donald N. Cook ◽  
Suzanne L. Kirby ◽  
Elizabeth Reap ◽  
Thomas C. Shea ◽  
...  
Keyword(s):  
T Cell ◽  
T Lymphocytes ◽  
Graft Versus Host Disease ◽  
Class Ii ◽  
Class I ◽  
Wild Type ◽  
Inhibitory Protein ◽  
Host Disease ◽  
Graft Versus Host

Abstract The routine use of bone marrow transplantation is limited by the occurrence of acute and chronic graft-versus-host disease (GVHD). Current approaches to decreasing the occurrence of GVHD after allogeneic transplantation use T-cell depletion, use immunosuppressive agents, or block costimulatory molecule function. The role of proteins in the recruitment of alloreactive lymphocytes has not been well characterized. Chemokines are a large family of proteins that mediate recruitment of mononuclear cells in vitro and in vivo. To investigate the role of T-cell production of the chemokine macrophage inhibitory protein-1 (MIP-1) in the occurrence of GVHD, splenocytes either from wild-type or from MIP-1−/− mice were administered to class I (B6.C-H2bm1) and class II disparate mice (B6-C-H2bm12). The incidence and severity of GVHD was markedly reduced in bm1 mice receiving splenocytes from MIP-1−/− mice as compared with mice receiving wild-type splenocytes. Bm1 mice receiving MIP-1−/− splenocytes had significantly less weight loss and markedly reduced inflammatory responses in the lung and liver than mice receiving C57BL/6 splenocytes. Bm1 mice receiving MIP-1−/− splenocytes had a markedly decreased production of antichromatin autoantibodies and impaired generation of bm1-specific T lymphocytes versus wild-type mice. However, MIP-1−/− splenocytes easily induced GVHD when administered to bm12 mice. This data show that blockade of chemokine production or function may provide a new approach to the prevention or treatment of GVHD but that chemokines that recruit both CD4+ and CD8+ lymphocytes may need to be targeted.

HLA class I and class II frequencies in patients with sarcoidosis from Croatia: role of HLA-B8, ?DRB1*0301, and ?DQB1*0201 haplotype in clinical variations of the disease

2007 ◽  
Vol 70 (4) ◽  
pp. 301-306 ◽  
Author(s):  
Z. Grubić ◽  
R. Žunec ◽  
T. Peroš-Golubičić ◽  
J. Tekavec-Trkanjec ◽  
N. Martinez ◽  
...  
Keyword(s):  
Hla Class I ◽  
Class Ii ◽  
Class I

T-cell recognition of a chimaeric class II/class I MHC molecule and the role of L3T4

Nature ◽  
1985 ◽  
Vol 317 (6036) ◽  
pp. 425-427 ◽  
Author(s):  
Hana Golding ◽  
James McCluskey ◽  
Terry I. Munitz ◽  
Ronald N. Germain ◽  
David H. Margulies ◽  
...  
Keyword(s):  
T Cell ◽  
Class Ii ◽  
Class I ◽  
Cell Recognition ◽  
Class I Mhc ◽  
T Cell Recognition
Sign in / Sign up

Export Citation Format

Share Document