PubMed Health⌕ Search

Biomedical subjects

D C Huang

Publications and source records attributed to D C Huang.

45 records · Page 3Linked to original sources
PubMed1993

Two genes present on a transposon-like structure in Lactococcus lactis are involved in a Clp-family proteolytic activity.

The lactose-protease plasmid pUCL22 of Lactococcus lactis subsp. lactis strain CNRZ270 contained two inverted copies of IS 1076 flanking a region of 3.7 kb. This internal region was sequenced and found to contain two large open reading frames, ORF1 and ORFP in opposite orientations. ORF1 consists of 2289 bp; the deduced 763-amino-acid sequence is similar to the ATPases of the ClpA family. It contains two well-conserved consensus ATP-binding sites. It was named ClpL. ORFP consists of 930 bp encoding a protein of 310 amino acids. No similarity with any known protein was found in GenBank data for ORFP. Increased ATP-dependent proteolytic activity was detected in extracts from Escherichia coli cells expressing the clpL and ORFP genes.

Adenosine Triphosphatases↗
PubMed1993

Plasma membrane-targeted ras GTPase-activating protein is a potent suppressor of p21ras function.

Although p21ras is localized to the plasma membrane, proteins it interacts with, such as the GTPase-activating proteins (GAPs) ras GAP and neurofibromin (NF1), are not, suggesting that one function of p21ras GTP may be to target such proteins to the plasma membrane. To investigate the effects of targeting ras GAP to the plasma membrane, ras C-terminal motifs sufficient for plasma membrane localization of p21ras were cloned onto the C terminus of ras GAP. Plasma membrane-targeted ras GAP is growth inhibitory to NIH 3T3 fibroblasts and COS cells. This growth inhibition correlates with GAP catalytic activity, since the plasma membrane-targeted C-terminal catalytic domain or the GAP-related domain of neurofibromin is inhibitory, whereas the similarly targeted N-terminal domain is not. Moreover, the inhibition is abrogated by the inactivating mutation L902I, which abolishes ras GAP catalytic activity. Coexpression of oncogenic mutant ras rescues cell viability, but the majority of rescued colonies are phenotypically untransformed. Furthermore, in focus assays, targeted ras GAP suppresses transformation by oncogenic mutant ras, and in reversion assays, targeted ras GAP can revert cells transformed by oncogenic mutant ras. Neither the targeted or nontargeted N-terminal domain nor the L902I mutant of ras GAP has any transforming activity. These data demonstrate that ras GAP can function as a negative regulator of ras and that plasma membrane localization potentiates this activity. However, if ras GAP is involved in the effector functions of p21ras, it can only be part of the effector complex for cell transformation.

Amino Acid Sequence↗
PubMed1992

Nonidentity between plasmid and chromosomal copies of ISS1-like sequences in Lactococcus lactis subsp. lactis CNRZ270 and their possible role in chromosomal integration of plasmid genes.

The nucleotide sequence of an insertion sequence (IS) observed during mating experiments using the lactose-protease plasmid, pUCL22, of Lactococcus (Lc.) lactis subsp. lactis CNRZ270, was found to be similar to that of ISS1 from Lc. lactis subsp. lactis ML3. The IS was named ISS1RS. The chromosome of this strain contains several copies of ISS1-like IS as assessed by hybridization. One of these copies was cloned and named ISS1CH. Its sequence differs from that of the plasmid-borne copy, and appears to be more closely related to ISS1N from Lc. lactis subsp. cremoris SK11. This suggests independent introduction of both ISS1 elements. Moreover, the observation of plasmid genes integrated in the CNRZ270 chromosome near ISS1CH suggests that their presence is the result of integration by a Campbell mechanism using both IS homologies. ISS1-like sequences were also found on plasmids of numerous Lc. lactis strains, as well as one out of seven Lactobacillus (Lb.) casei and one out of three Lb. plantarum strains examined.

Amino Acid Sequence↗
PubMed1991

A transposon-like element on the lactose plasmid of Lactococcus lactis subsp. lactis Z270.

An inverted repeat previously called IR was identified on the lactose plasmid of Lactococcus lactis subsp. lactis Z270 by self-annealing; it was now named IS1076. The two sequences were 3.3 kb apart. Both copies were cloned in E. coli, sequenced and found to be identical, except for an additional 44 bp direct repeat at the 5' end of the right-hand copy; they were thus respectively 1296 bp (IS1076R) and 1252 bp (IS1076L) long. Both elements end in near-perfect 39 bp inverted repeats, similar to the IS904 termini. Promoter consensus sequences and a RBS site precede an ORF1 of 384 amino acids. Subclones of IS1076R and IS1076L produced a new 44 kDa protein corresponding to the size of the ORF1. The distal part of the ORF1 coding region is very similar to the IS3 ORFI sequence and the IS904 ORF sequence, and the proximal part shows some homologies with IS3 ORFII. A three-base target is present as a direct repeat flanking the 5.9 kb genetic block including IS1076L, IS1076R and the internal region, resulting in a structure similar of that of a transposon.

Amino Acid Sequence↗
PubMed1988

Transposition of the Streptococcus lactis ssp. lactis Z270 lactose plasmid to pVA797: demonstration of an insertion sequence and its relationship to an inverted repeat sequence isolated by self-annealing.

The lactose plasmid pUCL22 of the single plasmid strain Streptococcus lactis ssp. lactis Z270 was demonstrated to fuse with the heterologous conjugative plasmid pVA797. The fusion of pUCL22 with pVA797 occurred by recombination between a specific sequence of pUCL22 and different sites of pVA797. The cointegrates of pUCL22::pVA797 were unstable: in the absence of lactose selection, they segregated plasmids that corresponded to pVA797 enlarged by one sequence of 1.2 kb, common to all derivative plasmids. This resolution sequence (RS) was shown to originate in the 9.7 kb BstEII restriction fragment of pUCL22 and to duplicate during replicon fusion. In addition, after nuclease S1 treatment of pUCL22 DNA, a self-annealing sequence was isolated; the two copies of this inverted repeat (IR) sequence were located on the 18 kb BamHI segment of the plasmid. This latter sequence was distinct from the RS with which it hybridized weakly. The RS was responsible for the transposition of the entire lactose plasmid; the role of the IR remains to be elucidated.

Conjugation, Genetic↗
PubMed1980

Use of intramuscular prostaglandin for failure of mid-trimester abortion by another method.

Eight investigators, using a common protocol, studied the use of intramuscular (15S)-15-methyl prostaglandin F2 alpha to abort midtrimester pregnancies which had failed treatment by other methods in 398 cases. Results of treatment of 3 subgroups, defined by reason for primary treatment failure, are presented. The combined efficacy rate was 96.2% with 79.6% of the abortions being complete. The mean time from starting intramuscular therapy to successful abortion was 7.35 hours. The incidence of gastrointestinal side-effects was lower than that previously reported for systemically administered prostaglandins. Serious complications were not appreciably different from those reported for commonly used methods of second trimester abortion except for a slightly higher incidence of excessive bleeding requiring blood replacement. Advantages of this method over currently used methods of treating failures of primary attempts to induce midtrimester abortion by pharmacologic means are discussed.

Abortion, Incomplete↗
PubMedDate not supplied

Intravenous prostacyclin in acute nonhemorrhagic stroke: a placebo-controlled double-blind trial.

The therapeutic efficacy of prostacyclin in nonhemorrhagic cerebral infarction was assessed in a placebo-controlled double-blind trial. A total of 80 patients with stroke onset within 24 hours were randomized into placebo (37 patients) and prostacyclin (43 patients) groups. Demographic data and risk factors were comparable. Patients in the prostacyclin group received a continuous i.v. infusion of prostacyclin at an average rate of 8.5 ng/kg/min for an average of 64 hours. The placebo group received vehicle only in a similar fashion. During treatment hemodynamic changes were more prominent in the patients receiving prostacyclin and included reduction of systolic and diastolic blood pressure and increase in pulse rate. In contrast there was only a slight (but significant) reduction of diastolic blood pressure in the placebo group. Neurologic deficit scores were determined on admission, at Day 3, and at Weeks 1, 2, and 4. Mean neurologic deficit scores upon entry were comparable in the placebo and prostacyclin groups, and a significant improvement in the score for neurologic deficit was noted in both. The placebo group tended to fare better throughout the study, with a significant difference in neurologic deficit score favoring the placebo group at Week 2 (p = 0.0048). Two patients in the placebo and one in the prostacyclin group died. The only difference in adverse reactions was flushing (6 patients in prostacyclin vs. 0 in placebo group, p less than 0.05). The results of this study suggest a lack of therapeutic efficacy of prostacyclin in a defined population of patients with nonhemorrhagic cerebral infarction.

Acute Disease↗
PubMedDate not supplied

Serum HDL level at acute stage of Kawasaki disease.

Kawasaki disease is a disease of acute vascular inflammation of unknown etiology and HDL is a known risk factor of vascular damage. So far, there is no specific serum marker for KD. The previous study has shown a remarkable change of serum HDL in the patients with KD. To find whether changes in serum HDL level is a specific serum marker for early diagnosis of KD, we measured the concentration of HDL, LDL, TC, TG and CRP immediately after admission and one week later in three groups of patients (56 patients with KD, 38 patients with clinical viral infection, and 42 patients with bacterial infection). There was a significant decrease of HDL and increase of TG immediately after admission in three groups of patients. HDL and TG did not return to normal one week later. HDL level is more adversely affected in severe diseases than in mild diseases. Our results indicated that low HDL level is noted in various acute infection and is not a specific serum marker in the early stage of Kawasaki disease. It is interesting that low HDL is a universal phenomenon in this series. Further research is needed to explain the mechanism of lipid alterations and its consequences.

Acute Disease↗