Disease relevance of S100a11

• The heat level of starved Ehrlich ascites carcinoma cells (endogenous) was almost constant and linear and depended on the cell number used in the experiments (about 1 cal/1 X 10(8) cells/hr) [1].
• Sensitization of tumor necrosis factor alpha-resistant human melanoma by tumor-specific in vivo transfer of the gene encoding endothelial monocyte-activating polypeptide II using recombinant vaccinia virus [2].
• Regulation of EMAP II by hypoxia [3].
• This report investigates the role of neovascularization in the pathogenesis of stromal keratitis by measuring the outcome of treatment with the potent anti-angiogenesis cytokine endothelial monocyte-activating polypeptide II (EMAP II) [4].
• We show that systemic and topical administration of EMAP II from the outset of infection resulted in markedly diminished levels of herpes simplex virus-induced angiogenesis and significantly reduced the severity of stromal keratitis lesions [4].

High impact information on S100a11

• Endothelial-monocyte activating polypeptide II, a novel antitumor cytokine that suppresses primary and metastatic tumor growth and induces apoptosis in growing endothelial cells [5].
• Protein QUPC 52 gives maximum binding with isomaltohexaose (IM6) (deltaF degrees = -5,340 cal/mol) and has about 70% of its total binding energy for isomaltotriose (IM3), but at most only 5% for isomaltose (IM2) or methyl alphaDglucoside [6].
• Endothelial monocyte-activating polypeptide II (EMAP II) is a proinflammatory cytokine and a chemoattractant for monocytes [7].
• On the other hand, heat evolution was directly related to the amount of glucose added to the medium but not to the number of cells (19 cal/mmol of glucose) [1].
• The amount of heat produced by the addition of glucose (19 cal/mmol) was equivalent to 40% of the theoretical value of energy released through glycolysis (47 cal/mmol) [1].

Chemical compound and disease context of S100a11

• The effect of the phosphatase inhibitor calyculin A (cal A) on the kinetic parameters of the Na+-coupled taurine uptake via the taurine transporter in the Ehrlich ascites tumour cells has been investigated [8].

Biological context of S100a11

• CONCLUSIONS: These studies demonstrated that EMAP is a novel protein in corneal endothelial cells that is capable of inducing programmed cell death [9].
• A statistically significant difference was found in the level of antibodies specific to EMAP between patients at high risk for corneal transplant rejection and control subjects (P<0.001) [9].
• The mouse calgizzarin gene was localized on mouse chromosome 5, region E-F [10].
• The murine calgizzarin like gene (Cal) encodes for a calcium binding protein, which belongs to the S100 family of EF-hand proteins [11].
• We have previously demonstrated that inhibition of neovascularization by endothelial monocyte-activating polypeptide (EMAP) II also attenuates fetal lung morphogenesis in vivo, and hypothesized that epithelial-mesenchymal interactions are regulated by vascular signals [12].

Anatomical context of S100a11

• The mature peptide of EMAP alone was capable of inducing the death of cultured endothelial cells, whereas the propeptide was inactive [9].
• Taken together, our results indicate that calgizzarin expression could be repressed by factors originated from pachytene spermatocytes and/or spermatids [10].
• In addition, using both RT-PCR analysis and whole-mount in situ hybridization on dissected gonads it was demonstrated that mouse calgizzarin expression starts at 13.5 dpc in the prenatal male gonad and at 16.5 dpc in the embryonic ovary, respectively [10].
• Calgizzarin is expressed in all adult tissues examined, including testis and ovary; however, a high mRNA level for calgizzarin in mouse testis is maintained until day 15 of postnatal development and then declines dramatically, whereas the expression pattern in the ovary remains constantly high [10].
• One of the isolated differentially expressed genes, named calgizzarin, belongs to the family of S100 calcium-binding proteins and shows a decreased expression in Sertoli cell-germ cell cocultures compared to cultured Sertoli cells alone [10].

Associations of S100a11 with chemical compounds

• The protein synthesis inhibitor cycloheximide potentiated EMAP-induced apoptosis in endothelial cells [9].
• Evaluation of the effect of temperature on receptor binding of androgen allowed the estimation of several thermodynamic parameters, including activation energies of association (4 kcal/mol) and dissociation (14 kcal/mol), the apparent free energy (-13 kcal/mol), enthalpy (-9 kcal/mol), and entropy (+14 cal/mol per K) [13].
• The calorimetric data yielded the following thermodynamic parameters for arachidonic acid: Kd = 4.4 microM, n = 0.8, delta G = -7370 cal/mol, delta H = -6770 cal/mol, and T delta S = +600 cal/mol [14].
• For oleic acid, the thermodynamic parameters were Kd = 2.4 microM, n = 0.9, delta G = -7770 cal/mol, delta H = -6050 cal/mol, and T delta S = +1720 cal/mol [14].
• The P67.6 carbohydrate conjugate of calicheamicin is selectively cytotoxic at <0.006 ng/mL of calicheamicin equivalents (cal equiv) toward HL-60 promyelocytic leukemia cells in tissue culture [15].

Other interactions of S100a11

• The resulting tryptic peptides were sequenced by tandem mass spectrometry, and based on the recovered partial amino acid sequences, three of the tumor specific protein markers were identified as calgranulin A (S100A8), calgranulin B (S100A9) and calgizzarin (S100A11) [16].
• Upregulation of macrophage migration inhibitory factor and calgizzarin by androgen in TM4 mouse Sertoli cells [17].

Analytical, diagnostic and therapeutic context of S100a11

• Doses of gem-ozo as low as 50 microg cal/kg given three times to mice bearing HL-60 xenografts routinely resulted in long-term, tumor-free survivors, while a nonbinding control conjugate was relatively inactive [18].
• In a murine allograft model of lung neovascularization and morphogenesis, embryonic lungs transplanted under the skin of immunocompromised mice receiving intraperitoneal EMAP II, had a 56% reduction in vessel density (P<0.0001) compared to control [19].
• Furthermore, through the use of in situ hybridization and immunohistochemistry, EMAP II is localized throughout the lung, with significant expression in the submyoepithelial area during the early stages of lung development when there is minimal vascular development [20].
• To unravel neurobiological mechanisms underlying normal anxiety as well as its pathologi- cal variations, animal models are indispensable tools [21].

References