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A model of the carbohydrate recognition domain CRD, residues 111-245, of
hamster galectin-3 has been made using homology modeling and dynamics
minimization methods. The model is based on the known x-ray structures of
bovine galectin-1 and human galectin-2. The oligosaccharides
NeuNAc-alpha2,3-Gal-beta1,4-Glc and GalNAc-alpha1, 3-
[Fuc-alpha1,2]-Gal-beta1,4-Glc, known to be specific high-affinity ligands
for galectin-3, as well as lactose recognized by all galectins were docked
in the galectin-3 CRD model structure and a minimized binding conformation
found in each case. These studies indicate a putative extended
carbohydrate-binding subsite in the hamster galectin- 3 involving Arg139,
Glu230, and Ser232 for NeuNAc-alpha2,3-; Arg139 and Glu160 for
fucose-alpha1,2-; and Arg139 and Ile141 for GalNAc-alpha1,3- substituents
on the primary galactose. Each of these positions is variable within the
whole galectin family. Two of these residues, Arg139 and Ser232, were
selected for mutagenesis to probe their importance in this newly identified
putative subsite. Residue 139 adopts main-chain dihedral angles
characteristic of an isolated bridge structural feature, while residue 232
is the C-terminal residue of beta- strand-11, and is followed immediately
by an inverse gamma-turn. A systematic series of mutant proteins have been
prepared to represent the residue variation present in the aligned
sequences of galectins-1, - 2, and -3. Minimized docked models were
generated for each mutant in complex with NeuNAc-alpha2,3-Gal-beta1,4-Glc,
GalNAc-alpha1, 3-[Fuc- alpha1,2]-Gal-beta1,4- Glc, and Gal-beta1,4-Glc.
Correlation of the computed protein-carbohydrate interaction energies for
each lectin- oligosaccharide pair with the experimentally determined
binding affinities for fetuin and asialofetuin or the relative potencies of
lactose and sialyllactose in inhibiting binding to asiolofetuin is
consistent with the postulated key importance of Arg139 in recognition of
the extended sialylated ligand.
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Nucleotide sequence analysis of the human salivary protein genes HIS1 and HIS2, and evolution of the STATH/HIS gene family 总被引:1,自引:0,他引:1
Human histatins are a family of low-M(r), neutral to very basic,
histidine-rich salivary polypeptides. They probably function as part of the
nonimmune host defense system in the oral cavity. A 39-kb region of DNA
containing the HIS1 and HIS2 genes was isolated from two human genomic
phage libraries as a series of overlapping clones. The nucleotide sequences
of the HIS1 gene and part of the HIS2(1) gene were determined. The
transcribed region of HIS1 spans 8.5 kb and contains six exons and five
introns. The HIS1 and HIS2(1) genes exhibit 89% overall sequence identity,
with exon sequences exhibiting 95% identity. The two loci probably arose by
a gene duplication event approximately 15-30 Mya. The HIS1 sequence data
were also compared with that of STATH. Human statherin is a low-M(r) acidic
phosphoprotein that acts as an inhibitor of precipitation of calcium
phosphate salts in the oral cavity. The HIS1 and STATH genes show nearly
identical overall gene structures. The HIS1 and STATH loci exhibit 77%-81%
sequence identity in intron DNA and 80%-88% sequence identity in noncoding
exons but only 38%-43% sequence identity in the protein-coding regions of
exons 4 and 5. These unusual data suggest that HIS1, HIS2, and STATH belong
to a single gene family exhibiting accelerated evolution between the HIS
and STATH coding sequences.
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Evolution of the Adh locus in the Drosophila willistoni group: the loss of an intron, and shift in codon usage 总被引:1,自引:0,他引:1
We report here the DNA sequence of the alcohol dehydrogenase gene (Adh)
cloned from Drosophila willistoni. The three major findings are as follows:
(1) Relative to all other Adh genes known from Drosophila, D. willistoni
Adh has the last intron precisely deleted; PCR directly from total genomic
DNA indicates that the deletion exists in all members of the willistoni
group but not in any other group, including the closely related saltans
group. Otherwise the structure and predicted protein are very similar to
those of other species. (2) There is a significant shift in codon usage,
especially compared with that in D. melanogaster Adh. The most striking
shift is from C to U in the wobble position (both third and first
position). Unlike the codon-usage-bias pattern typical of highly biased
genes in D. melanogaster, including Adh, D. willistoni has nearly 50% G + C
in the third position. (3) The phylogenetic information provided by this
new sequence is in agreement with almost all other molecular and
morphological data, in placing the obscura group closer to the melanogaster
group, with the willistoni group farther distant but still clearly within
the subgenus Sophophora.
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An exception to the generally conservative nature of plastid gene evolution
is the gene coding for the beta" subunit of RNA polymerase, rpoC2. Previous
work by others has shown that maize and rice have an insertion in the
coding region of rpoC2, relative to spinach and tobacco. To assess the
distribution of this extra coding sequence, we surveyed a broad
phylogenetic sample comprising 55 species from 17 angiosperm families by
using Southern hybridization. The extra coding sequence is restricted to
the grasses (Poaceae). DNA sequence analysis of 11 species from all five
subfamilies within the grass family demonstrates that the extra sequence in
the coding region of rpoC2 is a repetitive array that exhibits more than a
twofold increase in nucleotide substitution, as well as a large number of
insertion/deletion events, relative to the adjacent flanking sequences. The
structure of the array suggests that slipped-strand mispairing causes the
repeated motifs and adds to the mechanisms through which the coding
sequence of plastid genes are known to evolve. Phylogenetic analyses based
on the sequence data from grass species support several relationships
previously suggested by morphological work, but they are ambiguous about
broad relationships within the family.
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Background
The Burkholderia cepacia complex (Bcc) is a collection of nine genotypically distinct but phenotypically similar species. They show wide ecological diversity and include species that are used for promoting plant growth and bio-control as well species that are opportunistic pathogens of vulnerable patients. Over recent years the Bcc have emerged as problematic pathogens of the CF lung. Pseudomonas aeruginosa is another important CF pathogen. It is able to synthesise hydrogen cyanide (HCN), a potent inhibitor of cellular respiration. We have recently shown that HCN production by P. aeruginosa may have a role in CF pathogenesis. This paper describes an investigation of the ability of bacteria of the Bcc to make HCN. 相似文献47.
Little is known about the mode of cell killing associated with low-dose hyper-radiosensitivity, the radiation response that describes the enhanced sensitivity of cells to small doses of ionizing radiation. Using a technique that measures the activation of caspase 3, we have established a relationship between apoptosis detected 24 h after low-dose radiation exposure and low-dose hyper-radiosensitivity in four mammalian cell lines (T98G, U373, MR4 and 3.7 cells) and two normal human lymphoblastoid cell lines. The existence of low-dose hyper-radiosensitivity in clonogenic survival experiments was found to be associated with an elevated level of apoptosis after low-dose exposures, corroborating earlier observations (Enns et al., Mol. Cancer Res. 2, 557-566, 2004). We also show that enriching populations of MR4 and V79 cells with G(1)-phase cells, to minimize the numbers of G(2)-phase cells, abolished the enhanced low-dose apoptosis. These cell-cycle enrichment experiments strengthen the reported association between low-dose hyper-sensitivity and the radioresponse of G(2)-phase cells. These data are consistent with our current hypothesis to explain low-dose hyper-radiosensitivity, namely that the enhanced sensitivity of cells to low doses of ionizing radiation reflects the failure of ATM-dependent repair processes to fully arrest the progression of damaged G(2)-phase cells harboring unrepaired DNA breaks entering mitosis. 相似文献
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Kumar Narayanan Mohammed Omer Mohammed Arif Papani Sridhar Nitin Annarapu Shivaprasad Naidu Pankaj Jariwala Narasaraju Kavalipati Mukharjee Madivada Ramagiri Balaji Premchand M Sharath Reddy A Anil Krishna G Padmakumar EA 《Indian pacing and electrophysiology journal》2021,21(1):5-10
BackgroundLeft-sided ablation, targeting left inferior AV nodal extensions, is thought to be necessary for success in a small proportion of atrioventricular nodal re-entrant tachycardia (AVNRT) ablations; however Indian data are scarce in this regard.MethodsConsecutive cases of AVNRT undergoing slow pathway ablation in a single centre over an 18-month period were retrospectively analyzed. Left-sided ablation at the posteroseptal mitral annulus was performed if right-sided ablation failed to abolish AVNRT.ResultsFrom January 2017 to June 2018, out of 215 consecutive supraventricular tachycardia (SVT) cases, 154 (71.6%) were AVNRT (47.1 ± 13.1 years, 46.1% male). Trans-septal ablation was required in 5 (3.2%) cases (mean age 48.8 ± 9.4 years; 4 female, 1 male); all with typical (slow-fast) form of AVNRT. Compared with cases needing only right-sided ablation, radiofrequency time (50.8 ± 16.9 vs. 9.9 ± 8.5 min; p = 0.005) and procedure time (166.0 ± 35.0 vs 79.6 ± 35.9 min; p = 0.004) were significantly longer for trans-septal cases, while baseline intervals and tachycardia cycle length were not significantly different. Junctional ectopy was seen in only 2 of the 5 cases during left-sided ablation, but acute success (non-inducibility) was obtained in 3 cases. There were no instances of AV block. Over mean follow-up of 12.2 ± 4.0 months, clinical recurrence of AVNRT occurred in one case, while others remained arrhythmia-free without medication.ConclusionLeft-sided ablation was required in a small proportion of AVNRT ablations. Trans-septal approach targeting the posteroseptal mitral annulus was safe and yielded good mid-term clinical success. 相似文献
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Floris EA Udink ten Cate Nathalie Wiesner Uwe Trieschmann Markus Khalil Narayanswami Sreeram 《Indian pacing and electrophysiology journal》2010,10(6):248-256
A subset of children and adults with Wolff-Parkinson-White (WPW) syndrome develop dilated cardiomyopathy (DCM). Although DCM may occur in symptomatic WPW patients with sustained tachyarrhythmias, emerging evidence suggests that significant left ventricular dysfunction may arise in WPW in the absence of incessant tachyarrhythmias. An invariable electrophysiological feature in this non-tachyarrhythmia type of DCM is the presence of a right-sided septal or paraseptal accessory pathway. It is thought that premature ventricular activation over these accessory pathways induces septal wall motion abnormalities and ventricular dyssynchrony. LV dyssynchrony induces cellular and structural ventricular remodelling, which may have detrimental effects on cardiac performance. This review summarizes recent evidence for development of DCM in asymptomatic patients with WPW, discusses its pathogenesis, clinical presentation, management and treatment. The prognosis of accessory pathway-induced DCM is excellent. LV dysfunction reverses following catheter ablation of the accessory pathway, suggesting an association between DCM and ventricular preexcitation. Accessory pathway-induced DCM should be suspected in all patients presenting with heart failure and overt ventricular preexcitation, in whom no cause for their DCM can be found. 相似文献
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