automated-analytics/bionlp2004 · Datasets at Hugging Face

0

Since HUVECs released superoxide anions in response to TNF , and H2O2 induces VCAM-1 , PDTC may act as a radical scavenger .

Since <cell_line>HUVECs</cell_line> released superoxide anions in response to TNF , and H2O2 induces <protein>VCAM-1</protein> , PDTC may act as a radical scavenger .

1

Although ICAM-1 induction was unaffected , inhibitors of NADPH oxidase ( apocynin ) or cytochrome P-450 ( SKF525a ) suppressed VCAM-1 induction by TNF , revealing that several radical-generating systems are involved in its regulation .

Although <protein>ICAM-1</protein> induction was unaffected , inhibitors of <protein>NADPH oxidase</protein> ( apocynin ) or <protein>cytochrome P-450</protein> ( SKF525a ) suppressed <protein>VCAM-1</protein> induction by TNF , revealing that several radical-generating systems are involved in its regulation .

2

PDTC , apocynin , or SKF525a decreased adhesion of monocytic U937 cells to TNF-treated HUVECs ( by 75 % at 100 mumol/L PDTC ) .

PDTC , apocynin , or SKF525a decreased adhesion of <cell_line>monocytic U937 cells</cell_line> to <cell_line>TNF-treated HUVECs</cell_line> ( by 75 % at 100 mumol/L PDTC ) .

3

Inhibition by anti-VCAM-1 monoclonal antibody 1G11 indicated that U937 adhesion was VCAM-1 dependent and suppression by antioxidants was due to reduced VCAM-1 induction .

Inhibition by <protein>anti-VCAM-1 monoclonal antibody</protein> <protein>1G11</protein> indicated that <cell_line>U937</cell_line> adhesion was <protein>VCAM-1</protein> dependent and suppression by antioxidants was due to reduced <protein>VCAM-1</protein> induction .

4

( ABSTRACT TRUNCATED AT 250 WORDS )

5

Displacement of an E-box-binding repressor by basic helix-loop-helix proteins : implications for B-cell specificity of the immunoglobulin heavy-chain enhancer .

Displacement of an <protein>E-box-binding repressor</protein> by <protein>basic helix-loop-helix proteins</protein> : implications for B-cell specificity of the <dna>immunoglobulin heavy-chain enhancer</dna> .

6

The activity of the immunoglobulin heavy-chain ( IgH ) enhancer is restricted to B cells , although it binds both B-cell-restricted and ubiquitous transcription factors .

The activity of the <dna>immunoglobulin heavy-chain ( IgH ) enhancer</dna> is restricted to <cell_type>B cells</cell_type> , although it binds both <protein>B-cell-restricted and ubiquitous transcription factors</protein> .

7

Activation of the enhancer in non-B cells upon overexpression of the basic helix-loop-helix ( bHLH ) protein E2A appears to be mediated not only by the binding of E2A to its cognate E box but also by the resulting displacement of a repressor from that same site .

Activation of the <dna>enhancer</dna> in <cell_type>non-B cells</cell_type> upon overexpression of the <protein>basic helix-loop-helix ( bHLH ) protein</protein> <protein>E2A</protein> appears to be mediated not only by the binding of <protein>E2A</protein> to its cognate <dna>E box</dna> but also by the resulting displacement of a <protein>repressor</protein> from that same site .

8

We have identified a `` two-handed '' zinc finger protein , denoted ZEB , the DNA-binding specificity of which mimics that of the cellular repressor .

We have identified a <protein>`` two-handed '' zinc finger protein</protein> , denoted <protein>ZEB</protein> , the DNA-binding specificity of which mimics that of the <protein>cellular repressor</protein> .

9

By employing a derivative E box that binds ZEB but not E2A , we have shown that the repressor is active in B cells and the IgH enhancer is silenced in the absence of binding competition by bHLH proteins .

By employing a derivative <dna>E box</dna> that binds <protein>ZEB</protein> but not <protein>E2A</protein> , we have shown that the <protein>repressor</protein> is active in <cell_type>B cells</cell_type> and the <dna>IgH enhancer</dna> is silenced in the absence of binding competition by <protein>bHLH proteins</protein> .

10

Hence , we propose that a necessary prerequisite of enhancer activity is the B-cell-specific displacement of a ZEB-like repressor by bHLH proteins .

Hence , we propose that a necessary prerequisite of <dna>enhancer</dna> activity is the B-cell-specific displacement of a <protein>ZEB-like repressor</protein> by <protein>bHLH proteins</protein> .

11

Inhibition of NF-kappa B by sodium salicylate and aspirin [ see comments ]

Inhibition of <protein>NF-kappa B</protein> by sodium salicylate and aspirin [ see comments ]

12

The transcription factor nuclear factor-kappa B ( NF-kappa B ) is critical for the inducible expression of multiple cellular and viral genes involved in inflammation and infection including interleukin-1 ( IL-1 ) , IL-6 , and adhesion molecules .

The <protein>transcription factor</protein> <protein>nuclear factor-kappa B</protein> ( <protein>NF-kappa B</protein> ) is critical for the inducible expression of multiple <dna>cellular and viral genes</dna> involved in inflammation and infection including <protein>interleukin-1</protein> ( <protein>IL-1</protein> ) , <protein>IL-6</protein> , and <protein>adhesion molecules</protein> .

13

The anti-inflammatory drugs sodium salicylate and aspirin inhibited the activation of NF-kappa B , which further explains the mechanism of action of these drugs .

The anti-inflammatory drugs sodium salicylate and aspirin inhibited the activation of <protein>NF-kappa B</protein> , which further explains the mechanism of action of these drugs .

14

This inhibition prevented the degradation of the NF-kappa B inhibitor , I kappa B , and therefore NF-kappa B was retained in the cytosol .

This inhibition prevented the degradation of the <protein>NF-kappa B inhibitor</protein> , <protein>I kappa B</protein> , and therefore <protein>NF-kappa B</protein> was retained in the cytosol .

15

Sodium salicylate and aspirin also inhibited NF-kappa B -dependent transcription from the Ig kappa enhancer and the human immunodeficiency virus ( HIV ) long terminal repeat ( LTR ) in transfected T cells .

Sodium salicylate and aspirin also inhibited <protein>NF-kappa B</protein> -dependent transcription from the <dna>Ig kappa enhancer</dna> and the <dna>human immunodeficiency virus ( HIV ) long terminal repeat</dna> ( <dna>LTR</dna> ) in <cell_line>transfected T cells</cell_line> .

16

Effects of the antisense myb expression on hemin- and erythropoietin- induced erythroid differentiation of K562 cells .

Effects of the antisense myb expression on hemin- and erythropoietin- induced erythroid differentiation of <cell_line>K562 cells</cell_line> .

17

In order to elucidate the role of c-myb gene in erythroid differentiation of K562 cell induced by hemin ( Hm ) and erythropoietin ( Epo ) , we constructed recombinant plasmid that could produce antisense myb RNA after induction with dexamethasone .

In order to elucidate the role of <dna>c-myb gene</dna> in erythroid differentiation of <cell_line>K562 cell</cell_line> induced by <protein>hemin</protein> ( <protein>Hm</protein> ) and <protein>erythropoietin</protein> ( <protein>Epo</protein> ) , we constructed <dna>recombinant plasmid</dna> that could produce <rna>antisense myb RNA</rna> after induction with dexamethasone .

18

During treatment with Hm , K562 cells constitutively expressed c-myb mRNA , and 50 % of them began to synthesize hemoglobin ( Hb ) .

During treatment with <protein>Hm</protein> , <cell_line>K562 cells</cell_line> constitutively expressed <rna>c-myb mRNA</rna> , and 50 % of them began to synthesize <protein>hemoglobin</protein> ( <protein>Hb</protein> ) .

19

Expression of antisense myb RNA reduced the amount of c-myb mRNA , and the percentage of Hb-synthesizing cells was decreased to 20 % .

Expression of <rna>antisense myb RNA</rna> reduced the amount of <rna>c-myb mRNA</rna> , and the percentage of <cell_line>Hb-synthesizing cells</cell_line> was decreased to 20 % .

20

In the presence of Epo , c-myb mRNA declined and 20 % of K562 cells synthesized Hb regardless of antisense myb RNA expression .

In the presence of <protein>Epo</protein> , <rna>c-myb mRNA</rna> declined and 20 % of <cell_line>K562 cells</cell_line> synthesized <protein>Hb</protein> regardless of <rna>antisense myb RNA</rna> expression .

21

It is suggested that constitutive expression of c-myb mRNA is necessary for Hm -induced differentiation , and that a decrease in the amount of c-myb mRNA induced by antisense myb RNA expression suppresses Hm -induced differentiation .

It is suggested that constitutive expression of <rna>c-myb mRNA</rna> is necessary for <protein>Hm</protein> -induced differentiation , and that a decrease in the amount of <rna>c-myb mRNA</rna> induced by <rna>antisense myb RNA</rna> expression suppresses <protein>Hm</protein> -induced differentiation .

22

The amount of c-myb mRNA in K562 cells was reduced during the differentiation induced by Epo .

The amount of <rna>c-myb mRNA</rna> in <cell_line>K562 cells</cell_line> was reduced during the differentiation induced by <protein>Epo</protein> .

23

Expression of GATA-1 mRNA was almost constant during Hm -induced differentiation , but increased during Epo treatment .

Expression of <rna>GATA-1 mRNA</rna> was almost constant during <protein>Hm</protein> -induced differentiation , but increased during <protein>Epo</protein> treatment .

24

It is supposed that the mechanism of Hm -induced differentiation is distinguished from that of Epo -induced differentiation in K562 cells .

It is supposed that the mechanism of <protein>Hm</protein> -induced differentiation is distinguished from that of <protein>Epo</protein> -induced differentiation in <cell_line>K562 cells</cell_line> .

25

Prenatal immune challenge alters the hypothalamic-pituitary-adrenocortical axis in adult rats .

26

We investigated whether non-abortive maternal infections would compromise fetal brain development and alter hypothalamic-pituitary-adrenocortical ( HPA ) axis functioning when adult .

27

To study putative teratogenic effects of a T cell-mediated immune response versus an endotoxic challenge , 10-d-pregnant rats received a single intraperitoneal injection of 5 x 10 ( 8 ) human red blood cells ( HRBC ) or gram-negative bacterial endotoxin ( Escherichia coli LPS : 30 micrograms/kg ) .

To study putative teratogenic effects of a T cell-mediated immune response versus an endotoxic challenge , 10-d-pregnant rats received a single intraperitoneal injection of 5 x 10 ( 8 ) <cell_type>human red blood cells</cell_type> ( <cell_type>HRBC</cell_type> ) or gram-negative bacterial endotoxin ( Escherichia coli LPS : 30 micrograms/kg ) .

28

The adult male progeny ( 3 mo old ) of both experimental groups showed increased basal plasma corticosterone levels .

29

In addition , after novelty stress the HRBC group , but not the LPS group , showed increased ACTH and corticosterone levels .

In addition , after novelty stress the <cell_type>HRBC</cell_type> group , but not the <cell_line>LPS group</cell_line> , showed increased ACTH and corticosterone levels .

30

Both groups showed substantial decreases in mineralocorticoid ( MR ) and glucocorticoid receptor ( GR ) levels in the hippocampus , a limbic brain structure critical for HPA axis regulation , whereas GR concentrations in the hypothalamus were unchanged and in anterior pituitary were slightly increased .

Both groups showed substantial decreases in mineralocorticoid ( MR ) and glucocorticoid receptor ( GR ) levels in the hippocampus , a limbic brain structure critical for HPA axis regulation , whereas <protein>GR</protein> concentrations in the hypothalamus were unchanged and in anterior pituitary were slightly increased .

31

HRBC and LPS indeed stimulated the maternal immune system as revealed by specific anti-HRBC antibody production and enhanced IL-1 beta mRNA expression in splenocytes , respectively .

<cell_type>HRBC</cell_type> and LPS indeed stimulated the maternal immune system as revealed by specific <protein>anti-HRBC antibody</protein> production and enhanced IL-1 beta mRNA expression in <cell_type>splenocytes</cell_type> , respectively .

32

This study demonstrates that a T cell-mediated immune response as well as an endotoxic challenge during pregnancy can induce anomalies in HPA axis function in adulthood .

33

Clinically , it may be postulated that disturbed fetal brain development due to prenatal immune challenge increases the vulnerability to develop mental illness involving inadequate responses to stress .

34

A low NM23.H1 gene expression identifying high malignancy human melanomas .

A low <dna>NM23.H1 gene</dna> expression identifying high malignancy human melanomas .

35

The NM23 gene has been proposed as a metastasis-suppressor gene , and its use has been suggested as prognostic factor .

The <dna>NM23 gene</dna> has been proposed as a <dna>metastasis-suppressor gene</dna> , and its use has been suggested as prognostic factor .

36

NM23 was identified in a system of murine melanoma cell lines , in which an inverse relationship was found between NM23 expression and metastatic ability .

<protein>NM23</protein> was identified in a system of <cell_line>murine melanoma cell lines</cell_line> , in which an inverse relationship was found between <protein>NM23</protein> expression and metastatic ability .

37

In a human malignant melanoma study NM23 expression was found to be significantly lower in metastases that developed less than 24 months after diagnosis of the primary tumours .

In a human malignant melanoma study <protein>NM23</protein> expression was found to be significantly lower in metastases that developed less than 24 months after diagnosis of the primary tumours .

38

The present paper studies the expression of the NM23.H1 gene in cell lines which derive from primary or metastatic human malignant melanomas in relation to staging , infiltration degree , lymphocytic infiltration , cell morphology , cell pigmentation , karyotype , and disease-free survival .

The present paper studies the expression of the <dna>NM23.H1 gene</dna> in <cell_line>cell lines</cell_line> which derive from primary or metastatic human malignant melanomas in relation to staging , infiltration degree , lymphocytic infiltration , cell morphology , cell pigmentation , karyotype , and disease-free survival .

39

The level of mRNA expression of the NM23 gene is significantly lower in cell lines that derive from more infiltrating primary melanomas than in cell lines obtained from less infiltrating tumours .

The level of mRNA expression of the <dna>NM23 gene</dna> is significantly lower in <cell_line>cell lines</cell_line> that derive from more infiltrating primary melanomas than in <cell_line>cell lines</cell_line> obtained from less infiltrating tumours .

40

Moreover , cell lines derived from tumours of patients with a disease-free survival of more than 24 months ( 24-58 months ) express the NM23 gene at higher levels than cell lines obtained from melanomas of patients with a disease-free survival of less than 24 months ( 6-15 months ) .

Moreover , <cell_line>cell lines</cell_line> derived from tumours of patients with a disease-free survival of more than 24 months ( 24-58 months ) express the <dna>NM23 gene</dna> at higher levels than <cell_line>cell lines</cell_line> obtained from melanomas of patients with a disease-free survival of less than 24 months ( 6-15 months ) .

41

Activation of a novel serine/threonine kinase that phosphorylates c-Fos upon stimulation of T and B lymphocytes via antigen and cytokine receptors .

Activation of a novel <protein>serine/threonine kinase</protein> that phosphorylates <protein>c-Fos</protein> upon stimulation of <cell_type>T and B lymphocytes</cell_type> via antigen and <protein>cytokine receptors</protein> .

42

Ligation of Ag receptors in T and B lymphocytes initiates signal transduction cascades which alter the expression of genes that regulate cellular proliferation and differentiation .

Ligation of <protein>Ag receptors</protein> in <cell_type>T and B lymphocytes</cell_type> initiates signal transduction cascades which alter the expression of genes that regulate cellular proliferation and differentiation .

43

The transmission of signals from the membrane to the nucleus is mediated principally through the action of protein tyrosine and serine/threonine kinases .

The transmission of signals from the membrane to the nucleus is mediated principally through the action of <protein>protein tyrosine and serine/threonine kinases</protein> .

44

We have identified and characterized a novel serine/threonine kinase that phosphorylated the proto-oncogene product , c-Fos , and is termed Fos kinase .

We have identified and characterized a novel <protein>serine/threonine kinase</protein> that phosphorylated the <protein>proto-oncogene product</protein> , <protein>c-Fos</protein> , and is termed <protein>Fos kinase</protein> .

45

Fos kinase was rapidly activated after ligation of the CD3 and CD2 receptors in Jurkat and normal human T lymphocytes and in response to IL-6 and anti-IgM in the human B cell lines AF10 and Ramos , respectively .

<protein>Fos kinase</protein> was rapidly activated after ligation of the <protein>CD3 and CD2 receptors</protein> in <cell_line>Jurkat</cell_line> and <cell_type>normal human T lymphocytes</cell_type> and in response to <protein>IL-6</protein> and <protein>anti-IgM</protein> in the <cell_line>human B cell lines</cell_line> <cell_line>AF10</cell_line> and <cell_line>Ramos</cell_line> , respectively .

46

The phorbol ester , PMA , was also a potent inducer of Fos kinase activity in all of the above populations , suggesting that PKC plays a role in the regulation of this enzyme .

The phorbol ester , PMA , was also a potent inducer of <protein>Fos kinase</protein> activity in all of the above populations , suggesting that <protein>PKC</protein> plays a role in the regulation of this <protein>enzyme</protein> .

47

Fos kinase phosphorylates c-Fos at a site near the C-terminus , as well as a peptide derived from this region ( residues 359-370 , RKGSSSNEPSSD ) , and Fos peptide competitively inhibited c-Fos phosphorylation .

<protein>Fos kinase</protein> phosphorylates <protein>c-Fos</protein> at a site near the <protein>C-terminus</protein> , as well as a peptide derived from this region ( <protein>residues 359-370</protein> , <protein>RKGSSSNEPSSD</protein> ) , and Fos peptide competitively inhibited <protein>c-Fos</protein> phosphorylation .

48

Fos kinase was shown to be distinct from other identified serine/threonine kinases , including protein kinase A , protein kinase C , casein kinase II , MAP kinases , p70S6K and p90RSK .

<protein>Fos kinase</protein> was shown to be distinct from other identified <protein>serine/threonine kinases</protein> , including <protein>protein kinase A</protein> , <protein>protein kinase C</protein> , <protein>casein kinase II</protein> , <protein>MAP kinases</protein> , <protein>p70S6K</protein> and <protein>p90RSK</protein> .

49

Fos kinase was purified by anion exchange chromatography and exhibited an apparent M ( r ) = 65 , 000 and isoelectric point = 6.1 .

<protein>Fos kinase</protein> was purified by anion exchange chromatography and exhibited an apparent M ( r ) = 65 , 000 and isoelectric point = 6.1 .

50

Fos kinase may play a role in transcriptional regulation through its capacity to phosphorylate c-Fos at a site required for expression of the transcriptional transrepressive activity of this molecule .

<protein>Fos kinase</protein> may play a role in transcriptional regulation through its capacity to phosphorylate <protein>c-Fos</protein> at a site required for expression of the transcriptional transrepressive activity of this molecule .

51

Moreover , its rapid activation suggests it may have a wider role within signal transduction cascades in lymphocytes .

Moreover , its rapid activation suggests it may have a wider role within signal transduction cascades in <cell_type>lymphocytes</cell_type> .

52

Antigenic specificities of human CD4+ T-cell clones recovered from recurrent genital herpes simplex virus type 2 lesions .

Antigenic specificities of <cell_line>human CD4+ T-cell clones</cell_line> recovered from recurrent genital herpes simplex virus type 2 lesions .

53

Lesions resulting from recurrent genital herpes simplex virus ( HSV ) infection are characterized by infiltration of CD4+ lymphocytes .

Lesions resulting from recurrent genital herpes simplex virus ( HSV ) infection are characterized by infiltration of <cell_type>CD4+ lymphocytes</cell_type> .

54

We have investigated the antigenic specificity of 47 HSV-specific CD4+ T-cell clones recovered from the HSV-2 buttock and thigh lesions of five patients .

We have investigated the antigenic specificity of 47 <cell_line>HSV-specific CD4+ T-cell clones</cell_line> recovered from the HSV-2 buttock and thigh lesions of five patients .

55

Clones with proliferative responses to recombinant truncated glycoprotein B ( gB ) or gD of HSV-2 or purified natural gC of HSV-2 comprised a minority of the total number of HSV-specific clones isolated from lesions .

Clones with proliferative responses to <protein>recombinant truncated glycoprotein B</protein> ( <protein>gB</protein> ) or <protein>gD</protein> of HSV-2 or purified natural gC of HSV-2 comprised a minority of the total number of <cell_line>HSV-specific clones</cell_line> isolated from lesions .

56

The gC2- and gD2-specific CD4+ clones had cytotoxic activity .

The <cell_line>gC2- and gD2-specific CD4+ clones</cell_line> had cytotoxic activity .

57

The approximate locations of the HSV-2 genes encoding HSV-2 type-specific CD4+ antigens have been determined by using HSV-1 x HSV-2 intertypic recombinant virus and include the approximate map regions 0.30 to 0.46 , 0.59 to 0.67 , 0.67 to 0.73 , and 0.82 to 1.0 units .

The approximate locations of the HSV-2 genes encoding HSV-2 type-specific <protein>CD4+ antigens</protein> have been determined by using HSV-1 x HSV-2 intertypic recombinant virus and include the approximate map regions 0.30 to 0.46 , 0.59 to 0.67 , 0.67 to 0.73 , and 0.82 to 1.0 units .

58

The antigenic specificity of an HLA DQ2-restricted , HSV-2 type-specific T-cell clone was mapped to amino acids 425 to 444 of VP16 of HSV-2 by sequential use of an intertypic recombinant virus containing VP16 of HSV-2 in an HSV-1 background , recombinant VP16 fusion proteins , and synthetic peptides .

The antigenic specificity of an <cell_line>HLA DQ2-restricted , HSV-2 type-specific T-cell clone</cell_line> was mapped to <protein>amino acids 425 to 444</protein> of <protein>VP16</protein> of HSV-2 by sequential use of an intertypic recombinant virus containing <protein>VP16</protein> of HSV-2 in an HSV-1 background , <protein>recombinant VP16 fusion proteins</protein> , and synthetic peptides .

59

Each of the remaining four patients also yielded at least one type-specific T-cell clone reactive with an HSV-2 epitope mapping to approximately 0.67 to 0.73 map units .

Each of the remaining four patients also yielded at least one <cell_line>type-specific T-cell clone</cell_line> reactive with an HSV-2 epitope mapping to approximately 0.67 to 0.73 map units .

60

The antigenic specificities of lesion-derived CD4+ T-cell clones are quite diverse and include at least 10 epitopes .

The antigenic specificities of <cell_line>lesion-derived CD4+ T-cell clones</cell_line> are quite diverse and include at least 10 epitopes .

61

Human T-cell clones reactive with gC and VP16 are reported here for the first time .

<cell_line>Human T-cell clones</cell_line> reactive with <protein>gC</protein> and <protein>VP16</protein> are reported here for the first time .

62

Marked basophilia in acute promyelocytic leukaemia treated with all-trans retinoic acid : molecular analysis of the cell origin of the basophils .

Marked basophilia in acute promyelocytic leukaemia treated with all-trans retinoic acid : molecular analysis of the cell origin of the <cell_type>basophils</cell_type> .

63

We report a patient with acute promyelocytic leukaemia who developed marked basophilia during all-trans retinoic acid treatment .

64

We studied genomic DNA and RNA extracted from the patient 's peripheral leucocytes in order to determine the origin of the basophils .

We studied <dna>genomic DNA</dna> and RNA extracted from the patient 's <cell_type>peripheral leucocytes</cell_type> in order to determine the origin of the <cell_type>basophils</cell_type> .

65

The RAR alpha rearranged band in the Southern blot analysis and a chimaeric product of PML-RAR alpha by polymerase chain reaction were strongly visible before ATRA treatment , but at the time of maximal basophilia both of them were markedly diminished .

The <protein>RAR alpha</protein> rearranged band in the Southern blot analysis and a <protein>chimaeric product</protein> of <protein>PML-RAR alpha</protein> by polymerase chain reaction were strongly visible before ATRA treatment , but at the time of maximal basophilia both of them were markedly diminished .

66

These findings suggest that the basophils which appeared during the ATRA treatment are reactive in nature rather than a leukaemic clone .

These findings suggest that the <cell_type>basophils</cell_type> which appeared during the ATRA treatment are reactive in nature rather than a <cell_line>leukaemic clone</cell_line> .

67

Activation of the interleukin 6 gene by Mycobacterium tuberculosis or lipopolysaccharide is mediated by nuclear factors NF-IL6 and NF-kappa B [ published erratum appears in Proc Natl Acad Sci U S A 1995 Apr 11 ; 92 ( 8 ) : 3632 ]

Activation of the <dna>interleukin 6 gene</dna> by Mycobacterium tuberculosis or lipopolysaccharide is mediated by <protein>nuclear factors NF-IL6</protein> and <protein>NF-kappa B</protein> [ published erratum appears in Proc Natl Acad Sci U S A 1995 Apr 11 ; 92 ( 8 ) : 3632 ]

68

The host response to Mycobacterium tuberculosis includes granuloma formation at sites of infection and systemic symptoms .

69

Cytokines have been identified by immunohistochemistry in granulomas in animal models of bacillus Calmette-Guerin ( BCG ) infection and are released by mononuclear phagocytes upon stimulation by mycobacterial proteins .

<protein>Cytokines</protein> have been identified by immunohistochemistry in granulomas in animal models of bacillus Calmette-Guerin ( BCG ) infection and are released by <cell_type>mononuclear phagocytes</cell_type> upon stimulation by mycobacterial proteins .

70

In this regard , the cytokine interleukin 6 ( IL-6 ) may play a role in the clinical manifestations and pathological events of tuberculosis infection .

In this regard , the <protein>cytokine</protein> <protein>interleukin 6</protein> ( <protein>IL-6</protein> ) may play a role in the clinical manifestations and pathological events of tuberculosis infection .

71

We have demonstrated that lipoarabinomannan ( LAM ) from the mycobacterial cell wall , which was virtually devoid of lipopolysaccharide ( LPS ) , stimulated mononuclear phagocytes to release IL-6 in a dose-response manner .

We have demonstrated that <protein>lipoarabinomannan</protein> ( <protein>LAM</protein> ) from the mycobacterial cell wall , which was virtually devoid of lipopolysaccharide ( LPS ) , stimulated <cell_type>mononuclear phagocytes</cell_type> to release <protein>IL-6</protein> in a dose-response manner .

72

LAM and LPS were potent inducers of IL-6 gene expression in peripheral blood monocytes .

<protein>LAM</protein> and LPS were potent inducers of <dna>IL-6 gene</dna> expression in <cell_type>peripheral blood monocytes</cell_type> .

73

Both LAM -and LPS-inducible IL-6 promoter activity was localized to a DNA fragment , positions -158 to -49 , by deletion analysis and chloramphenicol acetyltransferase assay .

Both <protein>LAM</protein> -and <dna>LPS-inducible IL-6 promoter</dna> activity was localized to a <dna>DNA fragment</dna> , positions <dna>-158 to -49</dna> , by deletion analysis and <protein>chloramphenicol acetyltransferase</protein> assay .

74

Two nuclear factor NF-IL6 ( positions -153 to -145 and -83 to -75 ) and one nuclear factor NF-kappa B ( positions -72 to -63 ) motifs are present within this fragment .

Two <protein>nuclear factor NF-IL6</protein> ( positions <dna>-153 to -145</dna> and -83 to -75 ) and one <dna>nuclear factor NF-kappa B ( positions -72 to -63 ) motifs</dna> are present within this fragment .

75

Site-directed mutagenesis of one or more of these motifs within the IL-6 promoter demonstrated that each has positive regulatory activity and that they could act in a function- and orientation-independent manner .

Site-directed mutagenesis of one or more of these motifs within the <protein>IL-6</protein> promoter demonstrated that each has positive regulatory activity and that they could act in a function- and orientation-independent manner .

76

Deletion of all three elements abolished inducibility of IL-6 promoter activity by both LAM and LPS .

Deletion of all three elements abolished inducibility of <dna>IL-6 promoter</dna> activity by both <protein>LAM</protein> and LPS .

77

We conclude that the NF-IL6 and NF-kappa B sites mediate IL-6 induction in response to both LPS and LAM , acting as bacterial or mycobacterial response elements .

We conclude that the <dna>NF-IL6 and NF-kappa B sites</dna> mediate <protein>IL-6</protein> induction in response to both LPS and <protein>LAM</protein> , acting as <dna>bacterial or mycobacterial response elements</dna> .

78

Regulation of CD14 expression during monocytic differentiation induced with 1 alpha , 25-dihydroxyvitamin D3 .

Regulation of <protein>CD14</protein> expression during monocytic differentiation induced with 1 alpha , 25-dihydroxyvitamin D3 .

79

CD14 , a monocyte/macrophage receptor for the complex of LPS and LPS binding protein , is a differentiation marker for the monocyte/macrophage lineage .

<protein>CD14</protein> , a <protein>monocyte/macrophage receptor</protein> for the complex of LPS and <protein>LPS binding protein</protein> , is a differentiation marker for the <cell_type>monocyte/macrophage lineage</cell_type> .

80

We have analyzed the regulation of CD14 expression during 1 alpha , 25-dihydroxyvitamin D3 ( VitD3 ) -induced monocytic differentiation .

We have analyzed the regulation of <protein>CD14</protein> expression during 1 alpha , 25-dihydroxyvitamin D3 ( VitD3 ) -induced monocytic differentiation .

81

Using FACS , Northern blotting , and nuclear run-on analyses , we demonstrate that the up-regulation of CD14 expression during monocytic cell maturation is regulated mainly at the level of gene transcription , and that new protein synthesis is required for CD14 induction .

Using FACS , Northern blotting , and nuclear run-on analyses , we demonstrate that the up-regulation of <protein>CD14</protein> expression during monocytic cell maturation is regulated mainly at the level of gene transcription , and that new protein synthesis is required for <protein>CD14</protein> induction .

82

We have recently cloned the CD14 5 ' upstream sequence and demonstrated its tissue-specific promoter activity .

We have recently cloned the <dna>CD14 5 ' upstream sequence</dna> and demonstrated its <dna>tissue-specific promoter</dna> activity .

83

Using stable transfection of the monocytoid U937 cell line with a series of deletion mutants of the CD14 5 ' upstream sequence coupled to a reporter gene construct , we show that bp -128 to -70 is the critical region for the induction of CD14 expression .

Using stable transfection of the <cell_line>monocytoid U937 cell line</cell_line> with a series of deletion mutants of the <dna>CD14 5 ' upstream sequence</dna> coupled to a reporter gene construct , we show that <dna>bp -128 to -70</dna> is the critical region for the induction of <protein>CD14</protein> expression .

84

This region contains two binding sites for the Sp1 transcription factor .

This region contains two <dna>binding sites</dna> for the <protein>Sp1 transcription factor</protein> .

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A 3-bp mutation at the distal Sp1-binding site not only eliminates Sp1 interaction , but also abolishes most of the VitD3 induction of CD14 expression .

A 3-bp mutation at the distal <dna>Sp1-binding site</dna> not only eliminates <protein>Sp1</protein> interaction , but also abolishes most of the VitD3 induction of <protein>CD14</protein> expression .

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Electrophoretic mobility shift analysis does not detect a direct interaction of the CD14 distal Sp1-binding site with the vitamin D3 receptor and its partner , the retinoid X receptor .

Electrophoretic mobility shift analysis does not detect a direct interaction of the <protein>CD14</protein> distal <dna>Sp1-binding site</dna> with the <protein>vitamin D3 receptor</protein> and its partner , the <protein>retinoid X receptor</protein> .

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These data demonstrate that VitD3 induces CD14 indirectly through some intermediary factor , and suggest a critical role for Sp1 in this process .

These data demonstrate that VitD3 induces <protein>CD14</protein> indirectly through some <protein>intermediary factor</protein> , and suggest a critical role for <protein>Sp1</protein> in this process .

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DNA-binding and transcriptional regulatory properties of hepatic leukemia factor ( HLF ) and the t ( 17 ; 19 ) acute lymphoblastic leukemia chimera E2A-HLF .

DNA-binding and transcriptional regulatory properties of <protein>hepatic leukemia factor</protein> ( <protein>HLF</protein> ) and the t ( 17 ; 19 ) <protein>acute lymphoblastic leukemia chimera E2A-HLF</protein> .

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The t ( 17 ; 19 ) translocation in acute lymphoblastic leukemias results in creation of E2A-hepatic leukemia factor ( HLF ) chimeric proteins that contain the DNA-binding and protein dimerization domains of the basic leucine zipper ( bZIP ) protein HLF fused to a portion of E2A proteins with transcriptional activation properties .

The <dna>t ( 17 ; 19 )</dna> translocation in acute lymphoblastic leukemias results in creation of <protein>E2A-hepatic leukemia factor</protein> ( <protein>HLF</protein> ) <protein>chimeric proteins</protein> that contain the <protein>DNA-binding and protein dimerization domains</protein> of the <protein>basic leucine zipper ( bZIP ) protein</protein> <protein>HLF</protein> fused to a portion of <protein>E2A proteins</protein> with transcriptional activation properties .

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An in vitro binding site selection procedure was used to determine DNA sequences preferentially bound by wild-type HLF and chimeric E2A-HLF proteins isolated from various t ( 17 ; 19 ) -bearing leukemias .

An in vitro binding site selection procedure was used to determine DNA sequences preferentially bound by <protein>wild-type HLF</protein> and <protein>chimeric E2A-HLF</protein> proteins isolated from various <cell_line>t ( 17 ; 19 ) -bearing leukemias</cell_line> .

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All were found to selectively bind the consensus sequence 5'-GTTACGTAAT-3 ' with high affinity .

All were found to selectively bind the <dna>consensus sequence</dna> 5'-GTTACGTAAT-3 ' with high affinity .

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Wild-type and chimeric HLF proteins also bound closely related sites identified previously for bZIP proteins of both the proline -and acidic amino acid-rich ( PAR ) and C/EBP subfamilies ; however , E2A-HLF proteins were significantly less tolerant of certain deviations from the HLF consensus binding site .

Wild-type and <protein>chimeric HLF proteins</protein> also bound closely related sites identified previously for <protein>bZIP proteins</protein> of both the <protein>proline</protein> -and acidic amino acid-rich ( <protein>PAR</protein> ) and <protein>C/EBP subfamilies</protein> ; however , <protein>E2A-HLF</protein> proteins were significantly less tolerant of certain deviations from the <dna>HLF consensus binding site</dna> .

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These differences were directly attributable to loss of an HLF ancillary DNA-binding domain in all E2A-HLF chimeras and were further exacerbated by a zipper mutation in one isolate .

These differences were directly attributable to loss of an <dna>HLF ancillary DNA-binding domain</dna> in all <protein>E2A-HLF chimeras</protein> and were further exacerbated by a zipper mutation in one isolate .

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Both wild-type and chimeric HLF proteins displayed transcriptional activator properties in lymphoid and nonlymphoid cells on reporter genes containing HLF or C/EBP consensus binding sites .

Both <protein>wild-type</protein> and <protein>chimeric HLF proteins</protein> displayed <protein>transcriptional activator</protein> properties in <cell_type>lymphoid and nonlymphoid cells</cell_type> on <dna>reporter genes</dna> containing <dna>HLF or C/EBP consensus binding sites</dna> .

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But on reporter genes with nonoptimal binding sites , their transcriptional properties diverged and E2A-HLF competitively inhibited activation by wild-type PAR proteins .

But on <dna>reporter genes</dna> with <dna>nonoptimal binding sites</dna> , their transcriptional properties diverged and <protein>E2A-HLF</protein> competitively inhibited activation by <protein>wild-type PAR proteins</protein> .

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These findings establish a spectrum of binding site-specific transcriptional properties for E2A-HLF which may preferentially activate expression of select subordinate genes as a homodimer and potentially antagonize expression of others through heteromeric interactions .

These findings establish a spectrum of binding site-specific transcriptional properties for <protein>E2A-HLF</protein> which may preferentially activate expression of select subordinate genes as a homodimer and potentially antagonize expression of others through heteromeric interactions .

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ZAP-70 tyrosine kinase , CD45 , and T cell receptor involvement in UV- and H2O2-induced T cell signal transduction .

<protein>ZAP-70 tyrosine kinase</protein> , <protein>CD45</protein> , and <protein>T cell receptor</protein> involvement in UV- and H2O2-induced T cell signal transduction .

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Several mammalian responses to UV irradiation , including the activation of NF-kappa B , are believed to involve tyrosine phosphorylation .

Several mammalian responses to UV irradiation , including the activation of <protein>NF-kappa B</protein> , are believed to involve tyrosine phosphorylation .

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UV irradiation and H2O2 treatment of T lymphocytes induce protein tyrosine phosphorylation and Ca2+ signals similar to those observed following biological stimulation .

UV irradiation and H2O2 treatment of <cell_type>T lymphocytes</cell_type> induce protein tyrosine phosphorylation and Ca2+ signals similar to those observed following biological stimulation .