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Статті в журналах з теми "SLF gene"

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Автор: Grafiati

Опубліковано: 10 грудня 2022

Оновлено: 28 січня 2023

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1

Li, Wentao, and Roger T. Chetelat. "Unilateral incompatibility gene ui1.1 encodes an S-locus F-box protein expressed in pollen of Solanum species." Proceedings of the National Academy of Sciences 112, no. 14 (March 23, 2015): 4417–22. http://dx.doi.org/10.1073/pnas.1423301112.

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Анотація:

Unilateral interspecific incompatibility (UI) is a postpollination, prezygotic reproductive barrier that prevents hybridization between related species when the female parent is self-incompatible (SI) and the male parent is self-compatible (SC). In tomato and related Solanum species, two genes, ui1.1 and ui6.1, are required for pollen compatibility on pistils of SI species or hybrids. We previously showed that ui6.1 encodes a Cullin1 (CUL1) protein. Here we report that ui1.1 encodes an S-locus F-box (SLF) protein. The ui1.1 gene was mapped to a 0.43-cM, 43.2-Mbp interval at the S-locus on chromosome 1, but positional cloning was hampered by low recombination frequency. We hypothesized that ui1.1 encodes an SLF protein(s) that interacts with CUL1 and Skp1 proteins to form an SCF-type (Skp1, Cullin1, F-box) ubiquitin E3 ligase complex. We identified 23 SLF genes in the S. pennellii genome, of which 19 were also represented in cultivated tomato (S. lycopersicum). Data from recombination events, expression analysis, and sequence annotation highlighted 11 S. pennellii genes as candidates. Genetic transformations demonstrated that one of these, SpSLF-23, is sufficient for ui1.1 function. A survey of cultivated and wild tomato species identified SLF-23 orthologs in each of the SI species, but not in the SC species S. lycopersicum, S. cheesmaniae, and S. galapagense, pollen of which lacks ui1.1 function. These results demonstrate that pollen compatibility in UI is mediated by protein degradation through the ubiquitin–proteasome pathway, a mechanism related to that which controls pollen recognition in SI.

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2

Schwarzenberger, P., SE Spence, JM Gooya, D. Michiel, DT Curiel, FW Ruscetti, and JR Keller. "Targeted gene transfer to human hematopoietic progenitor cell lines through the c-kit receptor." Blood 87, no. 2 (January 15, 1996): 472–78. http://dx.doi.org/10.1182/blood.v87.2.472.bloodjournal872472.

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Анотація:

In this report, we describe a novel gene therapy approach for hematopoietic stem/progenitor cells using a specific receptor-mediated gene transfection procedure to target c-kit+ cell lines. The vector consists of plasmid DNA containing a luciferase reporter gene that is condensed by electrostatic forces with polylysine (PL) covalently linked to streptavidin (binds biotinylated ligand) and PL covalently linked to adenovirus (AD; to achieve endosomal lysis) with the final addition of biotinylated steel factor (SLF-biotin). Targeted transfection of growth factor-dependent hematopoietic progenitor cell lines that express c-kit showed specific luciferase gene expression over cell lines that did not express c-kit. This effect was dependent on the dose of SLF-biotin and was competed by excess SLF or with monoclonal antibodies that recognize c-kit and block the binding of SLF to its receptor. Maximum transfection efficiency (> 90%) requires a 2- hour incubation period of the vector with the cells, and maximum gene expression occurred 30 hours later. Removal of the endosomalytic agent, AD, from the vector resulted in the loss of gene expression. Vector targeting was versatile and could be changed by the addition of other biotinylated ligands. In principle, this vector should be broadly applicable to deliver genes to hematopoietic stem/progenitor cells in vitro and in vivo.

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3

Miyazawa, K., K. Toyama, A. Gotoh, PC Hendrie, C. Mantel, and HE Broxmeyer. "Ligand-dependent polyubiquitination of c-kit gene product: a possible mechanism of receptor down modulation in M07e cells." Blood 83, no. 1 (January 1, 1994): 137–45. http://dx.doi.org/10.1182/blood.v83.1.137.137.

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Анотація:

Abstract Quantities of proteins in cells are balanced by protein synthesis and degradation. Protein ubiquitination is an important adenosine- triphosphate dependent proteolytic pathway for “short-lived” proteins. We show that soluble steel-factor (SLF) stimulation at 37 degrees C rapidly induced polyubiquitination of c-kit protein in growth-factor- dependent human-myeloid cell line M07e, resulting in smeared, retarded migration of c-kit protein in sodium dodecyl sulfate-polyacrylamide gel electrophoresis in the molecular weight region of 145 kD. Receptor ubiquitination was almost completely absent when cells were treated with SLF at 4 degrees C or at 37 degrees C in the presence of 0.2% sodium azide, or when the cells were pretreated with anti-c-kit monoclonal antibody or genistein, a tyrosine-kinase inhibitor. This suggested that c-kit ubiquitination was ligand dependent and appeared to require intrinsic tyrosine-kinase activation of the c-kit protein. Flow-cytometric analysis of c-kit expression on the cell surface of M07e cells showed down modulation of c-kit within 5 minutes after soluble-SLF treatment at 37 degrees C. However, rapid receptor down modulation was almost completely suppressed when cells were treated with SLF at 4 degrees C or at 37 degrees C in the presence of 0.2% sodium azide, conditions that concomitantly suppressed polyubiquitination of c-kit protein. In addition, these conditions almost completely suppressed radiolabeled SLF (125I-SLF) internalization after ligand-receptor interaction. Pulse-chase studies of 35S-methionine-labeled c-kit protein showed that SLF stimulation at 37 degrees C strikingly enhanced c-kit degradation (T1/2; approximately 20 minutes) compared with that in cells stimulated with SLF at 4 degrees C or at 37 degrees C with 0.2% sodium azide. However, in the presence of chloroquine, which blocks lysosomal degradation, this ligand-induced c-kit degradation at 37 degrees C was only suppressed in part. These data suggest that SLF-induced polyubiquitination of the c- kit receptor protein may play a role in regulation of c-kit-encoded protein-receptor expression in M07e cells.

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4

Miyazawa, K., K. Toyama, A. Gotoh, PC Hendrie, C. Mantel, and HE Broxmeyer. "Ligand-dependent polyubiquitination of c-kit gene product: a possible mechanism of receptor down modulation in M07e cells." Blood 83, no. 1 (January 1, 1994): 137–45. http://dx.doi.org/10.1182/blood.v83.1.137.bloodjournal831137.

Повний текст джерела

Анотація:

Quantities of proteins in cells are balanced by protein synthesis and degradation. Protein ubiquitination is an important adenosine- triphosphate dependent proteolytic pathway for “short-lived” proteins. We show that soluble steel-factor (SLF) stimulation at 37 degrees C rapidly induced polyubiquitination of c-kit protein in growth-factor- dependent human-myeloid cell line M07e, resulting in smeared, retarded migration of c-kit protein in sodium dodecyl sulfate-polyacrylamide gel electrophoresis in the molecular weight region of 145 kD. Receptor ubiquitination was almost completely absent when cells were treated with SLF at 4 degrees C or at 37 degrees C in the presence of 0.2% sodium azide, or when the cells were pretreated with anti-c-kit monoclonal antibody or genistein, a tyrosine-kinase inhibitor. This suggested that c-kit ubiquitination was ligand dependent and appeared to require intrinsic tyrosine-kinase activation of the c-kit protein. Flow-cytometric analysis of c-kit expression on the cell surface of M07e cells showed down modulation of c-kit within 5 minutes after soluble-SLF treatment at 37 degrees C. However, rapid receptor down modulation was almost completely suppressed when cells were treated with SLF at 4 degrees C or at 37 degrees C in the presence of 0.2% sodium azide, conditions that concomitantly suppressed polyubiquitination of c-kit protein. In addition, these conditions almost completely suppressed radiolabeled SLF (125I-SLF) internalization after ligand-receptor interaction. Pulse-chase studies of 35S-methionine-labeled c-kit protein showed that SLF stimulation at 37 degrees C strikingly enhanced c-kit degradation (T1/2; approximately 20 minutes) compared with that in cells stimulated with SLF at 4 degrees C or at 37 degrees C with 0.2% sodium azide. However, in the presence of chloroquine, which blocks lysosomal degradation, this ligand-induced c-kit degradation at 37 degrees C was only suppressed in part. These data suggest that SLF-induced polyubiquitination of the c- kit receptor protein may play a role in regulation of c-kit-encoded protein-receptor expression in M07e cells.

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5

Yip-Schneider, MT, M. Horie, and HE Broxmeyer. "Transcriptional induction of pim-1 protein kinase gene expression by interferon gamma and posttranscriptional effects on costimulation with steel factor." Blood 85, no. 12 (June 15, 1995): 3494–502. http://dx.doi.org/10.1182/blood.v85.12.3494.bloodjournal85123494.

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Анотація:

Steel factor (SLF) synergizes with interferon gamma (IFN gamma) to stimulate proliferation of the human factor-dependent cell line MO7e. We examined the effects of IFN gamma and SLF treatment, alone or in combination, on the expression of a 33-kD cytoplasmic protein serine/threonine kinase designated pim-1 whose expression has been closely associated with proliferation induced by related myeloid cytokines. IFN gamma alone, but not SLF, stimulated expression of pim-1 RNA and protein in MO7e cells; compared with IFN gamma alone, costimulation with IFN gamma and SLF resulted in a twofold to threefold increase in pim-1 message and protein expression, correlating with synergistic effects on cell proliferation. Both IFN gamma and IFN gamma/SLF induced pim-1 mRNA in the absence of de novo protein synthesis. Nuclear run-on assays showed that, although IFN gamma alone increased the rate of pim-1 gene transcription, costimulation with IFN gamma and SLF did not further potentiate this effect; however, the stability of pim-1 message was significantly enhanced in the presence of both cytokines. An IFN gamma-responsive element within the 5′ flanking region of the pim-1 gene that could confer IFN gamma responsiveness on a heterologous promoter was identified. This sequence, designated PMGAS, formed a specific complex with Stat (signal transducers and activators of transcription) 1 alpha (the p91 subunit of the transcription factor ISGF3 [interferon-stimulated gene factor 3]) in IFN gamma-treated cell extracts, suggesting that the transcriptional effects of IFN gamma on pim-1 expression may be mediated by Stat 1 alpha.

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6

Ren, Yi, Qingzhu Hua, Jiayan Pan, Zhike Zhang, Jietang Zhao, Xinhua He, Yonghua Qin, and Guibing Hu. "SKP1-like protein, CrSKP1-e, interacts with pollen-specific F-box proteins and assembles into SCF-type E3 complex in ‘Wuzishatangju’ (Citrus reticulata Blanco) pollen." PeerJ 8 (December 22, 2020): e10578. http://dx.doi.org/10.7717/peerj.10578.

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Анотація:

S-ribonuclease (S-RNase)-based self-incompatibility (SI) mechanisms have been extensively studied in Solanaceae, Rosaceae and Plantaginaceae. S-RNase-based SI is controlled by two closely related genes, S-RNase and S-locus F-box (SLF), located at a polymorphic S-locus. In the SI system, the SCF-type (SKP1-CUL1-F-box-RBX1) complex functions as an E3 ubiquitin ligase complex for ubiquitination of non-self S-RNase. Pummelo (Citrus grandis) and several mandarin cultivars are suggested to utilize an S-RNase-based SI system. However, the molecular mechanism of the non-S-factors involved in the SI reaction is not straightforward in Citrus. To investigate the SCF-type E3 complex responsible for the SI reaction in mandarin, SLF, SKP1-like and CUL1 candidates potentially involved in the SI reaction of ‘Wuzishatangju’ (Citrus reticulata Blanco) were identified based on the genome-wide identification and expression analyses. Sixteen pollen-specific F-box genes (CrFBX1-CrFBX16), one pollen-specific SKP1-like gene (CrSKP1-e) and two CUL1 genes (CrCUL1A and CrCUL1B) were identified and cloned from ‘Wuzishatangju’. Yeast two-hybrid (Y2H) and in vitro binding assays showed that five CrFBX proteins could bind to CrSKP1-e, which is an ortholog of SSK1 (SLF-interacting-SKP1-like), a non-S-factor responsible for the SI reaction. Luciferase complementation imaging (LCI) and in vitro binding assays also showed that CrSKP1-e interacts with the N-terminal region of both CrCUL1A and CrCUL1B. These results indicate that CrSKP1-e may serve as a functional member of the SCF-type E3 ubiquitin ligase complex in ‘Wuzishatangju’.

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7

Faust, E. A., D. C. Saffran, D. Toksoz, D. A. Williams, and O. N. Witte. "Distinctive growth requirements and gene expression patterns distinguish progenitor B cells from pre-B cells." Journal of Experimental Medicine 177, no. 4 (April 1, 1993): 915–23. http://dx.doi.org/10.1084/jem.177.4.915.

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Анотація:

Long-term bone marrow cultures have been useful in determining gene expression patterns in pre-B cells and in the identification of cytokines such as interleukin 7 (IL-7). We have developed a culture system to selectively grow populations of B lineage restricted progenitors (pro-B cells) from murine bone marrow. Pro-B cells do not grow in response to IL-7, Steel locus factor (SLF), or a combination of the two. c-kit, the SLF receptor, and the IL-7 receptor are both expressed by pro-B cells, indicating that the lack of response is not simply due to the absence of receptors. Furthermore, SLF is not necessary for the growth of pro-B cells since they could be expanded on a stromal line derived from Steel mice that produces no SLF. IL-7 responsiveness in pre-B cells is associated with an increase in n-myc expression and is correlated with immunoglobulin (Ig) gene rearrangements. Although members of the ets family of transcription factors and the Pim-1 kinase are expressed by pro-B cells, n-myc is not expressed. Pro-B cells maintain Ig genes in the germline configuration, which is correlated with a low level of recombination activating genes 1 and 2 (Rag-1 and 2) mRNA expression, but high expression of sterile mu and terminal deoxynucleotidyl transferase. Pro-B cells are unable to grow separated from the stromal layer by a porous membrane, indicating that stromal contact is required for growth. These results suggest that pro-B cells are dependent on alternative growth signals derived from bone marrow stroma and can be distinguished from pre-B cells by specific patterns of gene expression.

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8

Lu, Li, Michael C. Heinrich, Li-Sheng Wang, Mu-Shui Dai, Amy J. Zigler, Lin Chai та Hal E. Broxmeyer. "Retroviral-Mediated Gene Transduction of c-kit Into Single Hematopoietic Progenitor Cells From Cord Blood Enhances Erythroid Colony Formation and Decreases Sensitivity to Inhibition by Tumor Necrosis Factor- and Transforming Growth Factor-β1". Blood 94, № 7 (1 жовтня 1999): 2319–32. http://dx.doi.org/10.1182/blood.v94.7.2319.419k14_2319_2332.

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Анотація:

The c-kit receptor and its ligand, steel factor (SLF), are critical for optimal hematopoiesis. We evaluated effects of transducing cord blood (CB) progenitor cells with a retrovirus encoding humanc-kit cDNA. CD34+ cells were sorted as a population or as 1 cell/well for cells expressing high levels of CD34+++ and different levels of c-kit (++, +, Lo/−), transduced and then cultured in the presence of granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-3 (IL-3), IL-6, erythropoietin (Epo) +/− SLF in the absence of serum. At a single-cell level, transduction with c-kit, but not with control (neo only), virus significantly increased colony formation, especially by erythroid and multipotential progenitors. The enhancing effect of c-kit transduction was inversely correlated with expression of c-kit protein before transduction. The greatest enhancing effects were noted in CD34+++kitLo/− cells transduced with c-kit. The stimulating effect was apparent even in the absence of exogenously added SLF, but in the presence of GM-CSF, IL-3, IL-6, and Epo. Enzyme-linked immunosorbent assay (ELISA) of SLF protein, reverse transcriptase-polymerase chain reaction (RT-PCR) analysis of SLF mRNA expression in CD34+ cells, and use of neutralizing antibodies to SLF and/or c-kit suggested the presence of endogenous, although probably very low level, expression of SLF by these progenitor cells. Transduction of c-kit significantly decreased sensitivity of progenitor cells to the inhibitory effects of transforming growth factor-β1 and tumor necrosis factor-.c-kit–transduced cells had increased expression ofc-kit protein and decreased spontaneous or cytokine-induced apoptosis. Our results suggest that transduced c-kit into selected progenitor cells can enhance proliferation and decrease apoptosis and that endogenous SLF may mediate this effect.

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9

Shubber, E. K., and Z. MT Jaffer. "Establishment of HPRT and DHFR Gene Mutation Assays as biomarkers In Sheep lung fibroblasts (SLF)." Journal of Biotechnology Research Center 4, no. 2 (June 1, 2010): 11–17. http://dx.doi.org/10.24126/jobrc.2010.4.2.111.

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Анотація:

The aim of this research is to establish a gene mutation assay for examining the integrity of animal cell genome for nuclear transfer technique. Lung fibroblasts which were expanded from 4 months old female lamb were selected as target cells. These cells were coded (SLF) as Sheep lung cells. Growth characterization, doubling time, chromosomal number and structural integrity were checked after their growth in RPMI-1640 medium. For HPRT-gene mutation assay, the cells were plated at density of 1×103cells/plate and grown in medium containing toxic concentrations of 6-thioguanine; while for DHFR -gene mutation assay, toxic concentration of methotrexate was used as a selective agent. Those cells were grown for 15 days; mutant colonies either 6TGr or MTXr were reinoculated in a selective medium for further 8 weeks for checking the stability of phenotypic expression of mutant cells. The results revealed that SLF cells has spontaneous frequencies of HPRT, and DHFR gene mutations equal to 16 and 22×10-3 event/ generation/ cell, respectivel.These levels are normal comparing with other animal cell types, and these assays could be applied on other somatic cells.

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10

Lu, L., M. Xiao, D. W. Clapp, Z. H. Li, and H. E. Broxmeyer. "High efficiency retroviral mediated gene transduction into single isolated immature and replatable CD34(3+) hematopoietic stem/progenitor cells from human umbilical cord blood." Journal of Experimental Medicine 178, no. 6 (December 1, 1993): 2089–96. http://dx.doi.org/10.1084/jem.178.6.2089.

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Анотація:

Umbilical cord blood is rich in hematopoietic stem and progenitor cells and has recently been used successfully in the clinic as an alternative source of engrafting and marrow repopulating cells. With the likelihood that cord blood stem/progenitor cells will be used for gene therapy to correct genetic disorders, we evaluated if a TK-neo gene could be directly transduced in a stable manner into single isolated subsets of purified immature hematopoietic cells that demonstrate self-renewed ability as estimated by colony replating capacity. Sorted CD34(3+) cells from cord blood were prestimulated with erythropoietin (Epo), steel factor (SLF), interleukin (IL)-3, and granulocyte-macrophage colony stimulating factor (GM-CSF) and transduced with the gene in two ways. CD34(3+) cells were incubated with retroviral-containing supernatant from TK-neo vector-producing cells, washed, and plated directly or resorted as CD34(3+) cells into single wells containing a single cell or 10 cells. Alternatively, CD34(3+) cells were sorted as a single cell/well and then incubated with viral supernatant. These cells were cultured with Epo, SLF, IL-3, and GM-CSF +/- G418. The TK-neo gene was introduced at very high efficiency into low numbers of or isolated single purified CD34(3+) immature hematopoietic cells without stromal cells as a source of virus or accessory cells. Proviral integration was detected in primary G418-resistant(R) colonies derived from single immature hematopoietic cells, and in cells from replated colonies derived from G418R-colony forming unit-granulocyte erythroid macrophage megakaryocyte (CFU-GEMM) and -high proliferative potential colony forming cells (HPP-CFC). This demonstrates stable expression of the transduced gene into single purified stem/progenitor cells with replating capacity, results that should be applicable for future clinical studies that may utilize selected subsets of stem/progenitor cells for gene therapy.

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11

Ana Cristina Silva Bomfim, Camila Severiano Vasques, Carolina Rocha Silva, Clara Santana Peixoto, Júlia de Castro de Souza, Sergiane Amaral Gadelha, Thereza Inês Barbosa Soares Flores, Thiago Kaique Nunes Monteiro, Thiago Santos Vieira, and André Bacellar Costa Lima. "Síndrome de Li-Fraumeni à Luz da Prática Clínica do Oncologista." Revista Científica Hospital Santa Izabel 6, no. 2 (August 30, 2022): 73–85. http://dx.doi.org/10.35753/rchsi.v6i2.277.

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Анотація:

A síndrome de Li-Fraumeni (SLF) consiste em um distúrbio autossômico dominante, associado a mutações no gene da proteína tumoral p53. Apresenta uma maior expressão em mulheres jovens e está associada à ocorrência de determinados tipos de câncer, tais como sarcomas, leucemias, tumores cerebrais, câncer de mama e carcinomas adrenocorticais. Esta síndrome não apresenta quadro clínico ou fenótipo específico, suas manifestações clínicas estão em linha com o tipo de câncer apresentado e seu diagnóstico é baseado em critérios clínicos e confirmado por testes genéticos que analisam a mutação do gene p53. Dessa forma, a detecção precoce da mutação, a realização de testes de rastreamento e o aconselhamento genético podem ser capazes de alterar a história natural da doença e, consequentemente, reduzir a mortalidade associada aos principais tipos de neoplasias associadas à síndrome. Assim como no quadro clínico, não há tratamento específico para tal diagnóstico. A abordagem oncológica será, portanto, de acordo com o tipo de câncer que o paciente desenvolve. Pacientes com SLF parecem apresentar uma maior sensibilidade para desenvolver neoplasias induzidas por radiação, devendo-se então, avaliar individualmente indicações de alguns exames diagnósticos de imagem e propostas terapêuticas envolvendo radiação. Diante do contexto de novas perspectivas diagnósticas, de rastreio e seguimento trazemos aqui uma atualização sobre a SLF, ilustrada sob o panorama de um caso clínico norteador.

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12

Mantel, C., Z. Luo, J. Canfield, S. Braun, C. Deng, and HE Broxmeyer. "Involvement of p21cip-1 and p27kip-1 in the molecular mechanisms of steel factor-induced proliferative synergy in vitro and of p21cip-1 in the maintenance of stem/progenitor cells in vivo." Blood 88, no. 10 (November 15, 1996): 3710–19. http://dx.doi.org/10.1182/blood.v88.10.3710.bloodjournal88103710.

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Анотація:

Steel factor (SLF) is a hematopoietic cytokine that synergizes with other growth factors to induce a greatly enhanced proliferative state of hematopoietic progenitor cells and factor-dependent cell lines. Even though the in vivo importance of SLF in the maintenance and responsiveness of stem and progenitor cells is well documented, the molecular mechanism involved in its synergistic effects are mainly unknown. Some factor-dependent myeloid cell lines respond to the synergistic proliferative effects of SLF plus other cytokines in a manner similar to that of normal myeloid progenitor cells from bone marrow and cord blood. We show here that SLF can synergize with granulocyte-macrophage colony-stimulating factor (GM-CSF) to induce an enhanced phosphorylation of the retinoblastoma gene product and a synergistic increase in the total intracellular protein level of the cyclin-dependent kinase inhibitor, p21cip-1, which is correlated with a simultaneous decrease in p27kip-1 in the human factor-dependent myeloid cell line, M07e. Moreover, these cytokines synergize to increase p21cip- 1 binding and decrease p27kip-1 binding to cyclin-dependent kinase-2 (cdk2), an enzyme required for normal cell cycle progression; these inverse events correlated with increased cdk2 kinase activity. It is also shown that exogenous purified p21cip-1 can displace p27kip-1 already bound to cdk2 in vitro. These data implicate increased p21cip-1 and decreased p27kip-1 intracellular concentrations and their stoichiometric interplay in the enhanced proliferative status of cells stimulated by the combination of SLF and GM-CSF. In support of these findings, it is shown that hematopoietic progenitor cells from mice lacking p21cip-1 are defective in SLF synergistic proliferative response in vitro. Moreover, the cycling status of marrow and spleen progenitors and absolute numbers of marrow progenitors were significantly decreased in the p21cip-1 -/-, compared with the +/+ mice. We conclude that the cdk threshold regulators p21cip-1 and p27kip- 1 play a critical role in the normal mitogenic response of M07e cells and murine myeloid progenitor cells to these cytokines and particularly in the SLF synergistic proliferative response that is important to the normal maintenance of the stem/progenitor cell compartment.

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13

Welham, M. J., and J. W. Schrader. "Steel factor-induced tyrosine phosphorylation in murine mast cells. Common elements with IL-3-induced signal transduction pathways." Journal of Immunology 149, no. 8 (October 15, 1992): 2772–83. http://dx.doi.org/10.4049/jimmunol.149.8.2772.

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Анотація:

Abstract The c-kit/W gene encodes a transmembrane protein tyrosine kinase, which is the receptor for Steel factor (SLF). SLF shares many general characteristics of hemopoietic growth factors, stimulating the survival, proliferation, and differentiation of stem and progenitor cells. We have investigated the tyrosine phosphorylation events that ensue after SLF binding to the c-kit protein using primary cultures of murine mast cells as a model system and have compared the effects of SLF and IL-3. Proteins that became phosphorylated on tyrosine after treatment of cells with SLF included c-kit itself, and major protein substrates designated p130, p122, p118, p115, p112, p100, p77, p55, p44, and p42. The majority of these proteins were cytosolic and maximally phosphorylated within 2 min of growth factor treatment. Combinations of immunoprecipitation and immunoblotting with antibodies specific for proteins known to be associated with signaling pathways demonstrated that none of the major tyrosine-phosphorylated species correlated with phospholipase C-gamma 1, GTPase activating protein, or phosphatidylinositol 3' kinase. However, stimulation with SLF led to a modest increase in tyrosine phosphorylation of the 85-kDa subunit of the phosphatidylinositol 3' kinase and increased association with a 150-kDa phosphotyrosyl protein, likely to be c-kit. Two species that did correlate with known elements were the 44- and 42-kDa polypeptides, shown to be members of the mitogen-activated protein kinase family. A subset of these proteins (p130, p115/112, p100, p55, p44, p42) were also tyrosine-phosphorylated when cells were stimulated by IL-3. MonoQ ion-exchange chromatography and two dimensional gel analyses were used to demonstrate that at least the p55, p44, and p42 substrates were identical, as well as some more minor species of molecular weights 50, 38, and 36 kDa, thus indicating common pathways of signaling in hemopoietic cells. Whereas in the case of SLF the dose-response characteristics of the proliferative response and the induction of tyrosine phosphorylation were similar, in the case of IL-3, much lower concentrations were required for maximal proliferation than maximal tyrosine phosphorylation. These studies form the basis for further molecular characterization of common components of signal transduction pathways in hemopoietic cells.

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14

Miyazawa, K., DA Williams, A. Gotoh, J. Nishimaki, HE Broxmeyer, and K. Toyama. "Membrane-bound Steel factor induces more persistent tyrosine kinase activation and longer life span of c-kit gene-encoded protein than its soluble form." Blood 85, no. 3 (February 1, 1995): 641–49. http://dx.doi.org/10.1182/blood.v85.3.641.bloodjournal853641.

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Alternative splicing of exon 6 results in the production of two isoforms of Steel factor (SLF): the membrane-bound and soluble forms. To investigate differences in the kinetics of c-kit tyrosine kinase activated by these two isoforms, we used a stromal cell line (SI/SI4) established from SI/SI homozygous murine embryo fetal liver and its stable transfectants containing either hSCF248 cDNA (including exon 6; secreted form) or hSCF220 cDNA (lacking exon 6; membrane-bound form) as the source of each isoform. Interaction of factor dependent myeloid cell line MO7e with stromal cells producing either isoform resulted in activated c-kit tyrosine kinase and induction of the same series of tyrosine phosphorylated cellular proteins in MO7e cells. However, SI4- h220 (membrane-bound form) induced more persistent activation of c-kit kinase than SI4-h248 (soluble form) did. Flow cytometric analysis and pulse-chase studies using [35S]methionine showed that SI4-h248 induced rapid downmodulation of cell-surface c-kit expression and its protein degradation in MO7e cells, whereas SI4-h220 induced more prolonged life span of c-kit protein. Addition of soluble recombinant human SLF to SI4- h220 cultures enhanced reduction of cell-surface c-kit expression and its protein degradation. Because the kinetics of c-kit inactivation strikingly fits with the protein degradation rates of c-kit under the conditions described above, rapid proteolysis of c-kit protein induced by soluble SLF stimulation may function as a “turn-off switch” for activated c-kit kinase.

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15

Ma, Chunhui, and Haiyong Qu. "Gametophytic self-incompatibility in Rosaceae fruit trees." Acta Scientiarum Polonorum Hortorum Cultus 18, no. 4 (August 7, 2019): 149–56. http://dx.doi.org/10.24326/asphc.2019.4.14.

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Rosaceae fruit trees are characterized by gametophytic self-incompatibility, with their production typically requiring artificial pollination or pollination tree is required in production. Both of these solutions cause reductions in production efficiency, and self-incompatibility has become a major issue in agricultural biology, and as such, has been extensively studied. In this review, we discuss the relationship between S-RNase content in the style and self-incompatibility, and the role of the SLF gene in stamen-determining factor. Considering mutations in self-compatibility-related genes and self-compatibility in polyploid fruit trees, we discuss the potential mechanisms of self-incompatibility. Based on a preliminary study of the role of pollen tube Ca2+ gradients in self-incompatibility in Pyrus, we propose a new mechanistic model of self-incompatibility taking into account the effect of Ca2+. We also discuss the potential for hormone regulation to be used to control self-incompatibility in Rosaceae fruit trees.

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16

Hong, Hui, Markiyan Samborskyy, Katsiaryna Usachova, Katharina Schnatz, and Peter F. Leadlay. "Sulfation and amidinohydrolysis in the biosynthesis of giant linear polyenes." Beilstein Journal of Organic Chemistry 13 (November 13, 2017): 2408–15. http://dx.doi.org/10.3762/bjoc.13.238.

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Clethramycin from Streptomyces malaysiensis DSM4137, and mediomycins (produced together with clethramycin from Streptomyces mediocidicus), are near-identical giant linear polyenes apparently constructed from, respectively, a 4-guanidinobutanoate or 4-aminobutanoate starter unit and 27 polyketide extender units, and bearing a specific O-sulfonate modification at the C-29 hydroxy group. We show here that mediomycins are actually biosynthesised not by use of a different starter unit but by direct late-stage deamidination of (desulfo)clethramycin. A gene (slf) encoding a candidate sulfotransferase has been located in both gene clusters. Deletion of this gene in DSM4137 led to accumulation of desulfoclethramycin only, instead of a mixture of desulfoclethramycin and clethramycin. The mediomycin gene cluster does not encode an amidinohydrolase, but when three candidate amidinohydrolase genes from elsewhere in the S. mediocidicus genome were individually expressed in Escherichia coli and assayed, only one of them (medi4948), located 670 kbp away from the mediomycin gene cluster on the chromosome, catalysed the removal of the amidino group from desulfoclethramycin. Subsequent cloning of medi4948 into DSM4137 caused mediomycins A and B to accumulate at the expense of clethramycin and desulfoclethramycin, respectively, a rare case where an essential biosynthetic gene is not co-located with other pathway genes. Clearly, both desulfoclethramycin and clethramycin are substrates for this amidinohydrolase. Also, purified recombinant sulfotransferase from DSM4137, in the presence of 3'-phosphoadenosine-5'-phosphosulfate as donor, efficiently converted mediomycin B to mediomycin A in vitro. Thus, in the final steps of mediomycin A biosynthesis deamidination and sulfotransfer can take place in either order.

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17

Kardile, Hemant Balasaheb, Solomon Yilma, and Vidyasagar Sathuvalli. "Molecular Approaches to Overcome Self-Incompatibility in Diploid Potatoes." Plants 11, no. 10 (May 17, 2022): 1328. http://dx.doi.org/10.3390/plants11101328.

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There has been an increased interest in true potato seeds (TPS) as planting material because of their advantages over seed tubers. TPS produced from a tetraploid heterozygous bi-parental population produces non-uniform segregating progenies, which have had limited uniformity in yield and quality in commercial cultivation, and, thus, limited success. Inbreeding depression and self-incompatibility hamper the development of inbred lines in both tetraploid and diploid potatoes, impeding hybrid development efforts. Diploid potatoes have gametophytic self-incompatibility (SI) controlled by S-locus, harboring the male-dependent S-locus F-box (SLF/SFB) and female-dependent Stylar-RNase (S-RNase). Manipulation of these genes using biotechnological tools may lead to loss of self-incompatibility. Self-compatibility can also be achieved by the introgression of S-locus inhibitor (Sli) found in the self-compatible (SC) natural mutants of Solanum chacoense. The introgression of Sli through conventional breeding methods has gained much success. Recently, the Sli gene has been cloned from diverse SC diploid potato lines. It is expressed gametophytically and can overcome the SI in different diploid potato genotypes through conventional breeding or transgenic approaches. Interestingly, it has a 533 bp insertion in its promoter elements, a MITE transposon, making it a SC allele. Sli gene encodes an F-box protein PP2-B10, which consists of an F-box domain linked to a lectin domain. Interaction studies have revealed that the C-terminal region of Sli interacts with most of the StS-RNases, except StS-RNase 3, 9, 10, and 13, while full-length Sli cannot interact with StS-RNase 3, 9, 11, 13, and 14. Thus, Sli may play an essential role in mediating the interactions between pollen and stigma and function like SLFs to interact with and detoxify the S-RNases during pollen tube elongation to confer SC to SI lines. These advancements have opened new avenues in the diploid potato hybrid.

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18

Zarubina, Kseniia I., Elena N. Parovichnikova, Vadim L. Surin, Olesia S. Pshenichnikova, Olga A. Gavrilina, Galina A. Isinova, Vera V. Troitskaya, et al. "Li–Fraumeni syndrome in adult patients with acute lymphoblastic leukemia." Terapevticheskii arkhiv 93, no. 7 (July 23, 2021): 763–69. http://dx.doi.org/10.26442/00403660.2021.07.200913.

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Background. LiFraumeni syndrome (LFS) is a rare, autosomal dominant, hereditary disorder that is characterized by an increased risk for certain types of cancer, acute lymphoblastic leukemia (ALL), particularly. Germline TP53 mutations are associated with LFS. Genetic counseling and follow-up is essential for patients with LFS and their relatives. Special therapeutic approaches are needed for treatment of oncological disease in these patients. The article presents a series of clinical cases of patients with ALL and SLF, considers general issues of diagnosis and treatment of adult patients with this hereditary genetic syndrome. Aim. Describe clinical observations of patients with acute lymphoblastic leukemia (ALL) and LFS and consider general issues of diagnosis and treatment of adult patients with LFS and ALL. Materials and methods. TP53 gene mutations were screened using Sanger sequencing in 180 de novo patients with Ph-negative (B- and T-cell) and Ph-positive ALL treated by Russian multicenter protocols (ALL-2009, ALL-2012, ALL-2016) at the National Research Center for Hematology, Moscow, Russia, and at the hematology departments of regional clinics of Russia (multicenter study participants). Results. TP53 gene mutations were found in 7.8% (n=14) of de novo ALL patients. In patients, whose biological material was available TP53 gene mutational status was determined in non-tumor cells (bone marrow and peripheral blood during remission, bone marrow samples after allogeneic hematopoietic stem cells transplantation and in tissue of non-hematopoietic origin) for discriminating germline mutations. The analysis included 5 patients (out of 14 with TP53 mutations), whose non-tumor biological material was available for research. Germline status was confirmed in 4 out of 5 B-cell ALL (n=3), T-cell ALL (n=1) investigated patients. Conclusion. Practical value of the research is the observation that the greater part of TP53 gene mutations in patients with Ph-negative B-cell ALL are germinal and associated with LFS.

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19

Moon, Sung, Jeong-Im Woo, Sejo Oh, Yoojin Lee, Okjin Ahn, and David Lim. "IL-10-mediated modulation of cochlear inflammation (P6228)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 115.10. http://dx.doi.org/10.4049/jimmunol.190.supp.115.10.

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Abstract Inflammatory response is commonly involved in the pathogenesis of various cochlear diseases such as acoustic trauma and cisplatin ototoxicity. Previously, we have demonstrated that the spiral ligament fibrocytes play a pivotal role in cochlear inflammation through secretion of chemokines such as CCL2 and CXCL2 in response to pro-inflammatory signals. In this study, we aim to determine molecular mechanism involved in negative modulation of cochlear inflammation. We found that IL-10 inhibits SLF’s CCL2 up-regulation and migration of THP-1 cells in response to SLF-derived molecules. The SLFs appeared to up-regulate HMOX1 expression via NRF-2 activation. The inhibitory effect of IL-10 was mimicked by CoPP and CORM-3 but was blocked by silencing of IL-10RA and HMOX1. IL-10 was found to inhibit binding of p65 NFκB to the enhancer region of the CCL2 gene. IL-10 deficiency appeared to enhance cochlear inflammation secondary to nontypeable H. influenzae-induced otitis media. Furthermore, we demonstrated that the cochlear macrophages serve as a local source of IL-10, which appeared to be primarily distributed in the stria vascularis. Our results suggest that cochlear macrophage-derived IL-10 modulates cochlear inflammation by inhibition of SLF’s CCL2 up-regulation through HMOX1-mediated CO production. This study is anticipated providing us with a novel strategy for the management of inflammation-associated cochlear diseases.

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20

Wang, C., A. Ahlford, N. Laxman, G. Nordmark, M.-L. Eloranta, I. Gunnarsson, E. Svenungsson, et al. "Contribution of IKBKE and IFIH1 gene variants to SLE susceptibility." Genes & Immunity 14, no. 4 (March 28, 2013): 217–22. http://dx.doi.org/10.1038/gene.2013.9.

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21

Morris, D. L., M. M. A. Fernando, K. E. Taylor, S. A. Chung, J. Nititham, M. E. Alarcón-Riquelme, L. F. Barcellos, et al. "MHC associations with clinical and autoantibody manifestations in European SLE." Genes & Immunity 15, no. 4 (March 6, 2014): 210–17. http://dx.doi.org/10.1038/gene.2014.6.

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22

Rhodes, B., S. Hunnangkul, D. L. Morris, L.-C. Hsaio, D. S. Cunninghame Graham, D. Nitsch, J. C. Whittaker, and T. J. Vyse. "The heritability and genetics of complement C3 expression in UK SLE families." Genes & Immunity 10, no. 5 (April 23, 2009): 525–30. http://dx.doi.org/10.1038/gene.2009.23.

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23

Li, X., T. S. Ptacek, E. E. Brown та J. C. Edberg. "Fcγ receptors: structure, function and role as genetic risk factors in SLE". Genes & Immunity 10, № 5 (7 травня 2009): 380–89. http://dx.doi.org/10.1038/gene.2009.35.

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24

Armstrong, D. L., A. Reiff, B. L. Myones, F. P. Quismorio, M. Klein-Gitelman, D. McCurdy, L. Wagner-Weiner, et al. "Identification of new SLE-associated genes with a two-step Bayesian study design." Genes & Immunity 10, no. 5 (May 14, 2009): 446–56. http://dx.doi.org/10.1038/gene.2009.38.

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25

Sengupta, M., S. Liang, H.-H. S. Potula, L.-J. Chang, and L. Morel. "The SLE-associated Pbx1-d isoform acts as a dominant-negative transcriptional regulator." Genes & Immunity 13, no. 8 (September 20, 2012): 653–57. http://dx.doi.org/10.1038/gene.2012.43.

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26

Martins, M., A. H. Williams, M. Comeau, M. Marion, J. T. Ziegler, B. I. Freedman, J. T. Merrill та ін. "Genetic association of CD247 (CD3ζ) with SLE in a large-scale multiethnic study". Genes & Immunity 16, № 2 (8 січня 2015): 142–50. http://dx.doi.org/10.1038/gene.2014.73.

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27

Armstrong, D. L., R. Zidovetzki, M. E. Alarcón-Riquelme, B. P. Tsao, L. A. Criswell, R. P. Kimberly, J. B. Harley, et al. "GWAS identifies novel SLE susceptibility genes and explains the association of the HLA region." Genes & Immunity 15, no. 6 (May 29, 2014): 347–54. http://dx.doi.org/10.1038/gene.2014.23.

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28

Wong, Mary S., Wayne J. Hawthorne, and Nicholas Manolios. "Gene therapy in diabetes." Self/Nonself 1, no. 3 (July 2010): 165–75. http://dx.doi.org/10.4161/self.1.3.12643.

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29

Blute, M. "Gene-Culture Coevolutionary Games." Social Forces 85, no. 1 (September 1, 2006): 151–66. http://dx.doi.org/10.1353/sof.2006.0115.

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30

Dalan, Burak, Ozlem Timirci-Kahraman, Seda Gulec-Yilma, Emre Murat Altinkilic, Selvi Duman, Huseyin Ayhan, and Turgay Isbir. "POTENTIAL PROTECTIVE ROLE OF SDF-1 AND CXCR4 GENE VARIANTS IN THE DEVELOPMENT OF DEMENTIA." Psychiatria Danubina 32, no. 1 (April 15, 2020): 92–96. http://dx.doi.org/10.24869/psyd.2020.92.

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31

Morris, D. L., R. R. Graham, L.-P. Erwig, P. M. Gaffney, K. L. Moser, T. W. Behrens, T. J. Vyse, and D. S. Cunninghame Graham. "Variation in the upstream region of P-Selectin (SELP) is a risk factor for SLE." Genes & Immunity 10, no. 5 (April 30, 2009): 404–13. http://dx.doi.org/10.1038/gene.2009.17.

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32

Molineros, J. E., X. Kim-Howard, H. Deshmukh, C. O. Jacob, J. B. Harley, and S. K. Nath. "Admixture in Hispanic Americans: its impact on ITGAM association and implications for admixture mapping in SLE." Genes & Immunity 10, no. 5 (April 23, 2009): 539–45. http://dx.doi.org/10.1038/gene.2009.30.

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33

Lin, Wei, Naihe Jing, M. Albert Basson, Andr�e Dierich, Jonathan Licht, and Siew-Lan Ang. "Synergistic activity of Sef and Sprouty proteins in regulating the expression ofGbx2 in the mid-hindbrain region." genesis 41, no. 3 (2005): 110–15. http://dx.doi.org/10.1002/gene.20103.

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34

Koo Dae-Hwan. "Gene Patents in the US." Seoul Law Review 16, no. 2 (February 2009): 13–38. http://dx.doi.org/10.15821/slr.2009.16.2.002.

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35

Stokoe, William C. "Language: Gene-Created or Handmade?" Sign Language Studies 1089, no. 1 (1995): 331–46. http://dx.doi.org/10.1353/sls.1995.0021.

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36

Cooney, C. M., G. R. Bruner, T. Aberle, B. Namjou-Khales, L. K. Myers, L. Feo, S. Li, et al. "46,X,del(X)(q13) Turner's syndrome women with systemic lupus erythematosus in a pedigree multiplex for SLE." Genes & Immunity 10, no. 5 (May 21, 2009): 478–81. http://dx.doi.org/10.1038/gene.2009.37.

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37

Díaz-Barreiro, A., M. Bernal-Quirós, I. Georg, C. Marañón, M. E. Alarcón-Riquelme, and C. Castillejo-López. "The SLE variant Ala71Thr of BLK severely decreases protein abundance and binding to BANK1 through impairment of the SH3 domain function." Genes & Immunity 17, no. 2 (January 28, 2016): 128–38. http://dx.doi.org/10.1038/gene.2016.1.

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38

Yang, W., P. Ng, M. Zhao, N. Hirankarn, C. S. Lau, C. C. Mok, T. M. Chan, et al. "Population differences in SLE susceptibility genes: STAT4 and BLK, but not PXK, are associated with systemic lupus erythematosus in Hong Kong Chinese." Genes & Immunity 10, no. 3 (February 19, 2009): 219–26. http://dx.doi.org/10.1038/gene.2009.1.

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39

White, David C., and Carmelo A. Milano. "Gene Therapy in Cardiovascular Disease." Annals of Surgery 238, Supplement (December 2003): S90—S97. http://dx.doi.org/10.1097/01.sla.0000097772.28752.38.

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40

Duxbury, Mark S., Evan Matros, Hiromichi Ito, Michael J. Zinner, Stanley W. Ashley, and Edward E. Whang. "Systemic siRNA-Mediated Gene Silencing." Transactions of the ... Meeting of the American Surgical Association CXXII, &NA; (2004): 265–74. http://dx.doi.org/10.1097/01.sla.0000140755.97224.9a.

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41

Mocellin, Simone, Maurizio Provenzano, Carlo Riccardo Rossi, Pierluigi Pilati, Donato Nitti, and Mario Lise. "DNA Array-Based Gene Profiling." Annals of Surgery 241, no. 1 (January 2005): 16–26. http://dx.doi.org/10.1097/01.sla.0000150157.83537.53.

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42

Nafees, Hina, Satyam Khare, Shilpi Jain та Shaifali Nandwani. "ASSOCIATION OF SDF-1β GENE SINGLE NUCLEOTIDE POLYMORPHISM IN TYPE 2 DIABETES MELLITUS PATIENTS IN NORTH INDIAN POPULATION". International Journal of Anatomy and Research 4, № 3.3 (30 вересня 2016): 2854–59. http://dx.doi.org/10.16965/ijar.2016.355.

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43

Raskov, Hans, Jacob H. Søby, Jesper Troelsen, Rasmus D. Bojesen, and Ismail Gögenur. "Driver Gene Mutations and Epigenetics in Colorectal Cancer." Annals of Surgery 271, no. 1 (January 2020): 75–85. http://dx.doi.org/10.1097/sla.0000000000003393.

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44

Hennessy, James. "Gene self-replication." Nature Chemistry 5, no. 12 (November 21, 2013): 984–85. http://dx.doi.org/10.1038/nchem.1815.

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45

Stewart, David B., Arthur S. Berg, and John P. Hegarty. "Single Nucleotide Polymorphisms of the tcdC Gene and Presence of the Binary Toxin Gene Predict Recurrent Episodes of Clostridium difficile Infection." Annals of Surgery 260, no. 2 (August 2014): 299–304. http://dx.doi.org/10.1097/sla.0000000000000469.

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46

Allen, Casey J., Anthony J. Griswold, Carl I. Schulman, Danny Sleeman, Joe U. Levi, Alan S. Livingstone, and Kenneth G. Proctor. "Global Gene Expression Change Induced by Major Thoracoabdominal Surgery." Annals of Surgery 266, no. 6 (December 2017): 981–87. http://dx.doi.org/10.1097/sla.0000000000001992.

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47

Al-Khami, Amir A., Shikhar Mehrotra, and Michael I. Nishimura. "Adoptive immunotherapy of cancer: Gene transfer of T cell specificity." Self/Nonself 2, no. 2 (April 2011): 80–84. http://dx.doi.org/10.4161/self.2.2.15832.

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48

Murakata, Ayano, Shinji Tanaka, Kaoru Mogushi, Mahmut Yasen, Norio Noguchi, Takumi Irie, Atsushi Kudo, Noriaki Nakamura, Hiroshi Tanaka, and Shigeki Arii. "Gene Expression Signature of the Gross Morphology in Hepatocellular Carcinoma." Annals of Surgery 253, no. 1 (January 2011): 94–100. http://dx.doi.org/10.1097/sla.0b013e3181f9bc00.

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49

Schueler, Silvio, and Heino Konrad. "Dynamische Generhaltung in Europas Wäldern: Paneuropäische Konzepte nehmen Gestalt an." Schweizerische Zeitschrift fur Forstwesen 167, no. 6 (June 1, 2016): 325–32. http://dx.doi.org/10.3188/szf.2016.0325.

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Dynamic gene conservation in European forests: Pan-European concepts shaping up Forests in Europe consist mainly of wild, undomesticated tree populations showing high genetic variation that has been shaped by postglacial migration and manifold adaptations to their local environments. To conserve this genetic diversity, many European countries have developed programs for the conservation of forest genetic resources, which consist not only of seed orchards but also of forest stands for in situ gene conservation. The long-term aim of the so called “dynamic gene conservation” is the maintenance of the most important ecological and, on a longer time scale, evolutionary processes. In the European cooperation project EUFGIS, Pan-European minimum requirements for units of dynamic gene conservation in forests were developed. On the basis of these criteria, a common database of all these identified units was established. Moreover, the representativeness of the nominated conservation units for ecological zones and continental hot spots of genetic diversity was analyzed, and the vulnerability of the network under climate change was investigated. This analysis showed that the present network of dynamic conservation units for various tree species contains significant gaps in its ecological and phylogenetic representativeness and indicates that up to 65% of the nominated conservation units of a target tree species will be highly vulnerable under climate change. Therefore, the network of gene conservation units needs to be extended, and additional transnational conservation actions including European assisted migration schemes should be considered.

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50

Oliver, Charles M. "Fiction, Film, and Faulkner: The Art of Adaptation by Gene D. Phillips." Studies in American Fiction 18, no. 1 (1990): 124–25. http://dx.doi.org/10.1353/saf.1990.0018.

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