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Biomedical subjects

L Xing

Publications and source records attributed to L Xing.

At least 91 records · Page 5Linked to original sources
PubMed1996

Signal transduction by DR3, a death domain-containing receptor related to TNFR-1 and CD95.

Tumor necrosis factor receptor-1 (TNFR-1) and CD95 (also called Fas or APO-1) are cytokine receptors that engage the apoptosis pathway through a region of intracellular homology, designated the "death domain." Another death domain-containing member of the TNFR family, death receptor 3 (DR3), was identified and was shown to induce both apoptosis and activation of nuclear factor kappaB. Expression of DR3 appears to be restricted to tissues enriched in lymphocytes. DR3 signal transduction is mediated by a complex of intracellular signaling molecules including TRADD, TRAF2, FADD, and FLICE. Thus, DR3 likely plays a role in regulating lymphocyte homeostasis.

Adaptor Proteins, Signal Transducing↗
PubMed1996

Iterative methods for inverse treatment planning.

Iterative algorithms used in imaging science are generalized to study inverse treatment planning in radiotherapy. These algorithms consist of iteratively changing trial incident fluence functions which eventually yield a dose distribution consistent with the prescribed distribution. Application of the algorithms is presented for test cases of a circular phantom with cylindrically symmetric dose distributions. A comparison of the iterative beam profiles with previous analytic solutions shows excellent agreement, indicating that iterative techniques are promising to create sophisticated treatment plans. The relationship between the algorithms and several existing inverse treatment planning methods is discussed.

Algorithms↗
PubMed1996

Antiinflammatory effect of Trichosanthes kirilowii Maxim, and its effective parts.

This study was carried out to elucidate the antiinflammatory effect of 50% ethanol extract obtained from the fruit of Trichosanthes kirilowii Maxm, and its effective parts. The cut dried fruit was separated into the whole fruit, seeds and remaining parts, and each part was extracted with 50% ethanol. The antiinflammatory activity of these extracts was investigated on acetic acid-induced vascular permeability in mice, carrageenin-induced edema and cotton pellet-induced granuloma formation in rats, as well as writhing symptoms in mice. The whole fruit and seed extractions showed an antiinflammatory activity and analgesic activity, but the other part did not when given perorally. These results suggest that the antiinflammatory effect and analgesic effect induced by ethanol extract of the fruit of T. kirilowii may be due to the seeds contained in the fruit.

Animals↗
PubMed1996

Accelerative effect of "nanshikon" and its constituents on the proliferation of granulation tissue in rats.

The present study was carried out to examine the accelerative effect of the ether extract obtained from "Nanshikon" on the proliferation of granulation tissue induced by cotton pellet in rats and to elucidate its active principles. Among naphthoquinone derivatives, the ether extract contained mostly teracrylshikonin. At corresponding doses based on the contents of the naphthoquinone derivatives in the ether extract, the accelerative potencies of teracrylshikonin, beta, beta-dimethylacrylshikonin, and a mixture of alpha-methyl-n-butylshikonin and isovalerylshikonin were about the same. Also, the accelerative potencies of these compounds were somewhat weaker than that of the ether extract. From these results, it is suggested that the accelerative effect of the ether extract on the proliferation of granulation tissue is mainly due to teracrylshikonin, beta, beta-dimethylacrylshikonin and a mixture of alpha-methyl-n-butylshikonin and isovalerylshikonin contained in the ether extract, and the accelerative effect induced by ether extract might be an additive effect of these naphthoquinone derivatives.

Animals↗
PubMed1995

cAMP response element-binding protein (CREB) interacts with transcription factors IIB and IID.

cAMP response element-binding protein (CREB) participates in both constitutive and cAMP-induced transcription of cAMP-responsive genes. CREB-mediated constitutive transcription requires only CREB-binding sites and a minimal promoter region (containing the TATA through start sequences), indicating that CREB interacts directly with components of the general transcription machinery. In this study, a coimmunoprecipitation assay was used to test for interaction of CREB with the general transcription factors (TF) TFIIB and TFIID and the core component of TFIID, TATA-binding protein (TBP). Human TFIIB and TBP, tagged with distinct epitopes (eTFIIB and eTBP), were expressed in and purified from Escherichia coli, and holo-eTFIID, containing eTBP, was obtained from the HeLa cell line LTR alpha 3. 35S-Labeled CREB, synthesized in vitro and incubated with eTFIIB, was coimmunoprecipitated with antibody recognizing eTFIIB, indicating that CREB specifically binds to TFIIB. 35S-CREB was coimmunoprecipitated with antibody against eTBP, but only when incubated with the holo-eTFIID complex, not with eTBP alone. TFIIB interacted with TBP, but CREB was not coprecipitated with the eTBP antibody when incubated with eTBP plus TFIIB, so CREB did not form a stable ternary complex with TFIIB and TBP. Conversely, depletion of TFIIB from the holo-TFIID preparation did not diminish the level of interaction between CREB and TFIID. Thus, CREB interacts independently with TFIIB and TFIID, but not directly with TBP. A protein kinase A phosphorylation site mutant of CREB and wild-type CREB exhibited equivalent interaction with TFIIB, indicating that this phosphorylation is not required. Consistent with the role of CREB in promoting constitutive or basal transcription, the constitutive activation domain of CREB was sufficient for interaction with both TFIIB and TFIID.

Cyclic AMP Response Element-Binding Protein↗
PubMed1994

Three distinct regions within the constitutive activation domain of cAMP regulatory element-binding protein (CREB) are required for transcription activation.

The transcription factor cAMP regulatory element-binding protein (CREB) mediates both constitutive and cAMP-induced gene expression through distinct, independently acting domains. The constitutive activation domain (CAD) (amino acids (aa) 165-252) encompasses and overlaps exon 9 of the CREB gene (E9, aa 180-243). In the present study, deletion of either the CAD or exon 9 from CREB-GAL4 (CRG) reduced constitutive activity to less than 2-fold, without affecting kinase inducible activity. However, fusion of the CAD to the GAL4 DNA binding domain (CAD-G4) stimulated transcription, whereas fusion of exon 9 sequences did not. Deletion of the amino-terminal flanking region of exon 9 (aa 165-180), but not COOH-terminal flanking sequences (aa 243-252), decreased constitutive activation in either the CAD-G4 or CRG background. Deletion of the previously characterized glutamine-rich region (Q3, aa 218-252) or of a region containing a hydrophobic cluster of amino acids (HC, aa 180-218) also reduced constitutive activation by either CAD-G4 or CRG. No single mutation of hydrophobic residues within HC impaired activity of the CAD, but double and triple mutations did, suggesting that multiple weak interactions are involved in function of the HC region. Thus, exon 9 of the CREB gene is necessary but not sufficient for constitutive activation. The CAD requires three distinct regions for function, suggesting that CREB may interact with multiple targets in the RNA polymerase II complex.

Amino Acid Sequence↗
PubMed1994

The endoplasmic reticular heat shock protein gp96 is transcriptionally upregulated in interferon-treated cells.

A cDNA clone complementary to an interferon (IFN)-induced mRNA approximately 3 kb in length was identified and sequenced revealing homology with the endoplasmic reticular heat shock protein/ATPase gp96. Both IFN-alpha and -gamma transcriptionally upregulate expression of this gene. gp96 transcripts, protein, and ATPase activity are shown to be enhanced as a result of IFN treatment in two human cell lines and this effect requires de novo protein synthesis. gp96 molecules have recently been implicated in the presentation of endogenous antigens. A number of the key elements in this pathway, the transporter proteins, the major histocompatibility complex (MHC)-linked units of the proteasomes and the MHC class I molecules are known to be IFN inducible. Our results show that yet another molecule suggested to play an accessory role in the endogenous presentation pathway is IFN inducible. Further, our studies represent the first demonstration of modulation of expression of a heat shock protein by a cytokine and identify a new enzymatic activity upregulated in IFN-treated cells.

Adenosine Triphosphatases↗
PubMed1994

Suppression of mitochondrial mRNA levels and mitochondrial function in cells responding to the anticellular action of interferon.

A lambda cDNA library prepared from polyadenylated RNA isolated from Daudi cells was differentially screened to isolate cDNAs that recognize mRNA whose levels are reduced following interferon (IFN) treatment. Southern blot and DNA sequence analysis of 20 cDNA clones that were isolated revealed that they represented mitochondrially encoded mRNAs for the following proteins: cytochrome c oxidase subunits II and III, ATPase 6, cytochrome b, and subunit 1 of the NADH dehydrogenase. Northern blot analysis employing these cDNAs and oligonucleotides generated to the remaining mitochondrially encoded mRNAs demonstrated that IFN-alpha treatment of Daudi cells mediates a time-dependent suppression of the level of all of the mitochondrially encoded mRNAs. Study of this IFN-mediated effect reveals that: (i) the suppression of the level of these mRNAs is dependent on protein synthesis, (ii) it can be observed to occur prior to any detectable effect on thymidine incorporation, (iii) the degree of suppression correlates with the sensitivity of the cells to the anticellular action of IFN, and (iv) the suppression of the level of these RNAs appears to result from an effect on the level of transcription rather than on the stability of these mRNAs. A study of the level of cellular respiration in IFN-treated Daudi cells reveals a clear suppression 3 h following IFN treatment.

Base Sequence↗
PubMed1994

[Immunological observation on chyluric patients with heat-clearing and hemostatic drugs].

In order to investigate the pathogenesis and therapeutic mechanism of chyluria, an experiment with a basic Heat-clearing and hemostatic prescription was conducted in treating 30 patients of chyluria. The result, 26 cases were cured completely. The cell-mediated and humoral immunity observation showed that OKT3 and OKT4 levels were commonly low in chyluric cases, and OKT8 as higher than normal value, the OKT4/OKT8 ratio was inverted before treatment. While OKT3 and OKT4 increased commonly, and OKT8 decreased with the OKT4/OKT8 ratio adjusted after treatment. Meanwhile, humoral immunity level was also commonly low before treatment, it increased after treatment.

Adult↗
PubMed1993

Involvement of 3',5'-cyclic adenosine monophosphate regulatory element binding protein (CREB) in both basal and hormone-mediated expression of the phosphoenolpyruvate carboxykinase (PEPCK) gene.

Transcription of the phosphoenolpyruvate carboxykinase (PEPCK) and PEPCK-chloramphenicol acetyltransferase (CAT) genes is induced by cAMP and glucocorticoids and is inhibited by insulin in H4IIE cells, as it is in liver. In contrast, PEPCK-CAT expression in HepG2 cells is not affected by insulin but is induced by cAMP, which in turn is repressed by glucocorticoids. Mutations were introduced into well defined transcription factor binding sites to investigate possible interactions between the cAMP regulatory element (CRE) binding protein (CREB) and glucocorticoid response unit (GRU) binding proteins. H4IIE rat hepatoma cells were transfected with PEPCK-CAT plasmids with or without an expression vector for protein kinase A (PKA). Glucocorticoid-induced CAT activity was dependent upon the GRU and was decreased in plasmids lacking the CRE. To determine the direct effects of CREB, the DNA binding and dimerization domain of GAL4 was substituted for that of CREB (CRG), and the PEPCK CRE was replaced with a GAL4 binding site (G4PEPCK-CAT). CRG elevated basal and glucocorticoid-induced activities of G4PEPCK-CAT equally and restored responsiveness to PKA. The basal activity of CRG was not diminished by concomitant treatment with PKA plus its inhibitor peptide, PKI, or by mutation of the PKA phosphorylation. Deletion of C-terminal regions of the CREB activation domain from CRG diminished basal activation without affecting induction by PKA. The glucocorticoid-induced level of CAT activity decreased in proportion to the reduced ability of CREB to activate basal transcription. Induction by glucocorticoid, in the absence or presence of PKA, was not affected by CRG, indicating that interaction of GRU-bound factors with CREB is not required for glucocorticoid induction of PEPCK. These results indicate that CREB is directly involved in basal and PKA-induced expression of PEPCK, and that CREB supports glucocorticoid-induced PEPCK expression through its positive effect on basal transcription.

Animals↗