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Journal articles on the topic 'Ko`mir'

Author: Grafiati

Published: 5 June 2025

Last updated: 1 August 2025

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1

Mirzoyeva, I.E, and SaydullayevaA. "O'ZBEKISTONDA KO'MIR KONLARI VA UNING ATROF- MUHITGA TA'SIRINING GEOGRAFIK JIHATLARI." PEDAGOGS international research journal 1, no. 1 (2022): 105–10. https://doi.org/10.5281/zenodo.5837489.

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<strong><em>Annotatsiya: </em></strong><em>Ushbu maqolada O‘zbekistondagi ko‘mir konlari va ularning tarqalish geografiyasi hamda ko‘mir konlarining ekologik ahvoli to‘g‘risida ma’lumot berilgan.</em> <strong><em>Аннотация:</em></strong><em> В статье представлена информация об угольных месторождениях Узбекистана и географии их распространения, а также об экологической ситуации на угольных месторождениях.</em> <strong><em>Annotation:</em></strong><em> This article provides information on coal deposits in Uzbekistan and the geography of their distribution, as

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2

Yang, Lei, Sheng He, Ling Ling, et al. "Crosstalk between miR-144/451 and Nrf2 during Recovery from Acute Hemolytic Anemia." Genes 14, no. 5 (2023): 1011. http://dx.doi.org/10.3390/genes14051011.

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miR-144/451 and nuclear factor (erythroid-derived 2)-like 2 (Nrf2) regulate two antioxidative systems that have been identified to maintain redox homeostasis in erythroid cells by removing excess reactive oxygen species (ROS). Whether these two genes coordinate to affect ROS scavenging and the anemic phenotype, or which gene is more important for recovery from acute anemia, has not been explored. To address these questions, we crossed miR-144/451 knockout (KO) and Nrf2 KO mice and examined the phenotype change in the animals as well as the ROS levels in erythroid cells either at baseline or un

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3

Mitsumura, Takahiro, Yoshiaki Ito, Tomoki Chiba, et al. "Ablation of miR-146b in mice causes hematopoietic malignancy." Blood Advances 2, no. 23 (2018): 3483–91. http://dx.doi.org/10.1182/bloodadvances.2018017954.

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Abstract Excessive and constitutive activation of nuclear factor-κB (NF-κB) leads to abnormal cell proliferation and differentiation, leading to the development of malignant tumors, including lymphoma. MicroRNA 146a (miR-146a) and miR-146b, both of which carry an identical seed sequence, have been shown to contribute to inflammatory diseases and tumors by suppressing the expression of key molecules required for NF-κB activation. However, the functional and physiological differences between miR-146a and miR-146b in disease onset have not been fully elucidated. In this study, we generated miR-14

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Itkin, Tomer, Aya Ludin, Shiri Gur-Cohen, et al. "Microrna-155 Promotes Hematopoietic Stem and Progenitor Cell Mobilization and Proliferation." Blood 120, no. 21 (2012): 214. http://dx.doi.org/10.1182/blood.v120.21.214.214.

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Abstract Abstract 214 MicroRNAs (miRNAs) are small non-coding RNAs involved in various physiological processes, including hematopoiesis. Although miRNAs are broadly studied with regards to normal and malignant leukocyte development, the role of miRNAs in hematopoietic stem and progenitor (HSPC) migration and mobilization is poorly understood. Currently, induction of HSPC mobilization from the bone marrow (BM) to the peripheral blood (PB) is the major mean to harvest HSPCs for clinical transplantation. Recently, several miRNAs were found to be upregulated in macaque G-CSF-mobilized CD34+ HSPCs,

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Ishibashi, Shigeki, Naosuke Kamei, Yuji Tsuchikawa, et al. "Myelin-Specific microRNA-23a/b Cluster Deletion Inhibits Myelination in the Central Nervous System during Postnatal Growth and Aging." Genes 15, no. 4 (2024): 402. http://dx.doi.org/10.3390/genes15040402.

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Microribonucleic acids (miRNAs) comprising miR-23a/b clusters, specifically miR-23a and miR-27a, are recognized for their divergent roles in myelination within the central nervous system. However, cluster-specific miRNA functions remain controversial as miRNAs within the same cluster have been suggested to function complementarily. This study aims to clarify the role of miR-23a/b clusters in myelination using mice with a miR-23a/b cluster deletion (KO mice), specifically in myelin expressing proteolipid protein (PLP). Inducible conditional KO mice were generated by crossing miR-23a/b clusterfl

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6

Xiong, Chuanfeng, Wei Huang, Xiaoli Nie, et al. "Microrna-191 Regulates T-Cell Clonal Expansion during Graft-Versus-Host Disease." Blood 134, Supplement_1 (2019): 4433. http://dx.doi.org/10.1182/blood-2019-130179.

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Allogeneic hematopoietic cell transplantation is a potentially curative treatment choice for a wide variety of hematological malignancies. However, graft-versus-host disease (GVHD), which is mediated by donor alloreactive T cells, limits the success of this procedure. Previous studies have demonstrated that several microRNAs (miRs) modulate graft-versus-host disease. miR-191 was previously reported to be able to support T cell survival after TCR stimulation. We hypothesize that miR191 regulates T cell response during GVHD. To test this hypothesis, we first studied miR-191 expression in allorea

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7

Lara, Patricia, Araceli Aguilar-González, Francisco Martín, Cristina Mesas, Javier Moreno, and Ana R. Rama. "Exploring miR-21 Knock-Out Using CRISPR/Cas as a Treatment for Lung Cancer." Genes 16, no. 2 (2025): 133. https://doi.org/10.3390/genes16020133.

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Background: Lung cancer is a leading cause of cancer-related deaths worldwide. Its high incidence and poor prognosis demonstrate the need to investigate new therapies. The PI3K/AKT pathway is activated in carcinogenic processes such as invasion, proliferation, and drug resistance. MiR-21 is a microRNA overexpressed in numerous types of cancer and which activates PI3K/AKT pathway by down-regulating its main targets, PTEN and PDCD4. CRISPR is a revolutionary gene-editing technology that allows genes to be deleted. The aim of this study was to use CRISPR/Cas9 technology as an option to reduce car

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8

Fayziyev, Rabim. "O'ZBEKISTON RESPUBLIKASIDA KO'MIR QAZIB OLISH HAJMINI MATEMATIK MODELLASHTIRISH VA PROGNOZLASH." Innovations in Science and Technologies 2, no. 3 (2025): 139–47. https://doi.org/10.5281/zenodo.15015443.

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Ushbu maqolada 2010-2023 yillardagi O‘zbekiston Respublikasida ko‘mir qazib olish hajmi dinamikasi ko‘rsatkichlari asosida, shu davrlardagi hamda 2010 yildan 2017 yilgacha va undan keyingi davrlar uchun matematik modellari tuzilgan. 2024 yildan 2030 yilgacha prognoz ko‘rsatkichlari aniqlangan. Shuningdek, o‘rganilayotgan davrda ko‘mir qazib olish hajmining o‘sish dinamikasi tahlil qilingan.

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9

Grants, Jennifer, Joanna Wegrzyn, David Knapp, et al. "Single Cell-Resolution Analysis of HSC Dysfunction in Mir-146a knockout Mice." Blood 130, Suppl_1 (2017): 714. http://dx.doi.org/10.1182/blood.v130.suppl_1.714.714.

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Abstract MicroRNA miR-146a is frequently depleted in myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML). Loss of miR-146a may be an initiating event in tumorigenesis, as miR-146a loss in mouse models is sufficient to cause features of MDS and eventual progression to AML. To define how miR-146a loss initiates tumorigenesis, we analyzed hematopoietic stem cell (HSC) function from miR-146a knockout (KO) mice prior to onset of an overt malignant phenotype. Tracking cell division kinetics, proliferation, and differentiation of single long-term HSC (LT-HSC; EPCR+CD45+CD48-CD150+) in cul

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10

Samani, Adrienne, Rylie M. Hightower, Andrea L. Reid, et al. "miR-486 is essential for muscle function and suppresses a dystrophic transcriptome." Life Science Alliance 5, no. 9 (2022): e202101215. http://dx.doi.org/10.26508/lsa.202101215.

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miR-486 is a muscle-enriched microRNA, or “myomiR,” that has reduced expression correlated with Duchenne muscular dystrophy (DMD). To determine the function of miR-486 in normal and dystrophin-deficient muscles and elucidate miR-486 target transcripts in skeletal muscle, we characterized mir-486 knockout mice (mir-486 KO). mir-486 KO mice developed disrupted myofiber architecture, decreased myofiber size, decreased locomotor activity, increased cardiac fibrosis, and metabolic defects were exacerbated in mir-486 KO:mdx5cv (DKO) mice. To identify direct in vivo miR-486 muscle target transcripts,

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11

Xu, Jiawei, Lanya Fu, Junyao Deng, et al. "miR-301a Deficiency Attenuates the Macrophage Migration and Phagocytosis through YY1/CXCR4 Pathway." Cells 11, no. 24 (2022): 3952. http://dx.doi.org/10.3390/cells11243952.

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(1) Background: the miR-301a is well known involving the proliferation and migration of tumor cells. However, the role of miR-301a in the migration and phagocytosis of macrophages is still unclear. (2) Methods: sciatic nerve injury, liver injury models, as well as primary macrophage cultures were prepared from the miR-301a knockout (KO) and wild type (WT) mice to assess the macrophage’s migration and phagocytosis capabilities. Targetscan database analysis, Western blotting, siRNA transfection, and CXCR4 inhibition or activation were performed to reveal miR301a’s potential mechanism. (3) Result

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12

Zitzer, Nina C., Patricia A. Taylor, Apollinaire Ngankeu, et al. "MiR-155 Impacts T Cell Migration in Acute Graft-Versus-Host Disease (aGVHD)." Blood 126, no. 23 (2015): 3080. http://dx.doi.org/10.1182/blood.v126.23.3080.3080.

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Abstract Introduction: We reported that microRNA-155 (miR-155) expression is upregulated in donor T cells during aGVHD and mice receiving miR-155 knock-out (KO) donor splenocytes do not exhibit lethal GVHD and have improved survival as compared to mice receiving wild type (WT) splenocytes.1 While we showed that miR-155 does not affect the allo-reactive proliferative potential of T cells, a significant decrease in the expression of the homing receptors CCR5, CXCR4, and S1P1 was found on miR-155-KO T cells, suggesting that the loss of miR-155 could impair the migration of donor T cells to aGVHD

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13

Jansing, Johanna Christine, Jan Fiedler, Andreas Pich, et al. "miR-21-KO Alleviates Alveolar Structural Remodeling and Inflammatory Signaling in Acute Lung Injury." International Journal of Molecular Sciences 21, no. 3 (2020): 822. http://dx.doi.org/10.3390/ijms21030822.

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Acute lung injury (ALI) is characterized by enhanced permeability of the air–blood barrier, pulmonary edema, and hypoxemia. MicroRNA-21 (miR-21) was shown to be involved in pulmonary remodeling and the pathology of ALI, and we hypothesized that miR-21 knock-out (KO) reduces injury and remodeling in ALI. ALI was induced in miR-21 KO and C57BL/6N (wildtype, WT) mice by an intranasal administration of 75 µg lipopolysaccharide (LPS) in saline (n = 10 per group). The control mice received saline alone (n = 7 per group). After 24 h, lung function was measured. The lungs were then excised for proteom

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Mohammed, Zahraa abdulmohsin, and Gregorio Gomez. "miR-155 has positive and negative roles on cytokine production in mast cells." Journal of Immunology 202, no. 1_Supplement (2019): 54.7. http://dx.doi.org/10.4049/jimmunol.202.supp.54.7.

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Abstract Mast cells play a critical role in allergic inflammation by releasing preformed mediators such as histamine and serine neutral proteases, biosynthesizing lipid mediators like prostaglandins and leukotrienes, and synthesizing new cytokines. MicroRNA-155 (miR-155) plays a key regulatory role in the pathogenesis of allergy. The aim of this study was to investigate the biological functions of miR-155 on mast cell mediator release. MiR-155 was increased in human skin mast cells following FcɛRI crosslinking. To explore the role of miR-155 on mast cells function, we used bone marrow-derived

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15

Paralkar, Vikram R., Lance Palmer, Peng Xu, et al. "Erythroid miRNA-144/451 Binds Many mRNAs but Regulates Only a Small Subset." Blood 128, no. 22 (2016): 1198. http://dx.doi.org/10.1182/blood.v128.22.1198.1198.

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Abstract MicroRNAs (miRNAs) are small RNAs that bind Argonaute (Ago) family proteins and recruit them to target mRNAs based on seed sequence complementarity, thereby causing mRNA degradation and/or translational repression. Multiple miRNAs are dynamically expressed during erythropoiesis. Deletion of miR-144/451, the most abundantly expressed erythroid miRNA gene, causes anemia and increased red cell sensitivity to oxidant stress, in part by de-repressing the target mRNA Ywhaz. However, the total number of mRNAs targeted by miR-144/451 is unknown. To identify erythroblast miR-144/451 target gen

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16

Bouamar, Hakim, Long Wang, Manoela Ortega, An-Ping Lin, Daifeng Jiang, and Ricardo Aguiar. "Heightened DNA Damage Response and p53 Activation In MiR-155 Null Cells Are Context Specific and Aid Dependent." Blood 122, no. 21 (2013): 2279. http://dx.doi.org/10.1182/blood.v122.21.2279.2279.

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Abstract The germinal center (GC) reaction includes two critical events: somatic hypermutation (SHM) and class switch DNA recombination (CSR). These processes are tightly controlled, thus preventing excessive DNA injury which could lead to loss of normal B lymphocytes as well as the survival of cells with oncogenic DNA lesions. MicroRNA-155 (miR-155) plays an important role in immune cell biology; miR-155 knock-out (KO) mice have a defective mature B cell development characterized by a decreased number of GC B cells, whereas the Eμ-miR-155 transgenic mouse model develops and oligoclonal prolif

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17

Zhao, Jimmy L., Dinesh S. Rao, Mark Boldin, Konstantin Taganov, and David Baltimore. "MicroRNA-146a Deficiency Leads to Increased Myeloid Cell Proliferation and Activation." Blood 118, no. 21 (2011): 2815. http://dx.doi.org/10.1182/blood.v118.21.2815.2815.

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Abstract Abstract 2815 NF-κB is a key regulator of inflammation and the immune activation against pathogens. On the other hand, constitutive and dysregulated NF-κB activation has been shown to lead to hematologic malignancies. Thus, NF-κB activity has to be properly regulated to achieve this delicate balance. Recent studies on microRNA-146a (miR-146a) suggest it to be an important negative regulator of NF-κB activation by targeting TRAF6 and IRAK1. To characterize the function of miR-146a in the context of NF-κB activation in the hematopoietic system, we have created a knockout (KO) mouse with

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18

Liu, Siqi, Baojun Zhang, Regina Lin, Chaoran Li, and Qi-Jing Li. "miR-23a supports survival of activated CD4+ T cells by maintaining reactive oxygen species equilibrium (IRM5P.638)." Journal of Immunology 194, no. 1_Supplement (2015): 59.3. http://dx.doi.org/10.4049/jimmunol.194.supp.59.3.

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Abstract To identify key miRNAs that regulate CD4+ T cell responses, we profiled miRNA expression in CD4+ T cells at different phases post-antigen stimulation. As miR-23a is a miRNA that correlated strongly with effector CD4+ T cell expansion, we generated a T-cell specific miR-23a knockout mouse line (23T-KO). We found that miR-23a in T cells is essential for effective anti-bacteria protection, as the loss of effector T cells during the early phase of antigen activation rendered 23aT-KO mice susceptible to high-dose listeria infection. As early as a few hours post-activation in vitro, naïve 2

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Abduvaliyeva, Muqaddam Jumanazarovna, Muyassar Boboyorovna Xolboyeva, and Adolat Ilhom qizi Musurmonova. "OG'IR METALLARNI SORBSIYALASH UCHUN SORBENTLAR SINTEZI." JOURNAL OF UNIVERSAL SCIENCE RESEARCH 1, no. 2 (2023): 125–27. https://doi.org/10.5281/zenodo.7626490.

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Aktivlangan ko’mir - o’rik, gilos va yong’oq danaklari po’chog’idan tayyorlangan sorbentlarning sintezi ketma-ket uch bosqichda amalga oshirildi: suv bug'i oqimida danak po’choqlarining pirolizi; ko’mir kukunini suv bug’i bilan tozalash; olingan ko’mirni presslash va sorbent shakliga keltirish. Tabletka shaklidagi sorbentni og’ir metallar sorbtsiyasida qo’llanildi va element tahlili o’tkazildi.

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20

Li, Liuhui, Jinglin Zhang, Chenyang Lu, et al. "MicroRNA-7a2 Contributes to Estrogen Synthesis and Is Modulated by FSH via the JNK Signaling Pathway in Ovarian Granulosa Cells." International Journal of Molecular Sciences 23, no. 15 (2022): 8565. http://dx.doi.org/10.3390/ijms23158565.

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MicroRNA-7a2 (miR-7a2) plays fundamental roles in the female reproductive axis, and estrogen is indispensable for maintaining ovary function. However, the interaction between miR-7a2 and ovarian function is unclear. The present study aimed to determine whether and how miR-7a2 functions in estrogen synthesis. Firstly, the results verified that miR-7a was highly expressed in ovarian granulosa cells. The knockout (KO) of miR-7a2 caused infertility and abnormal ovarian function in mice. Concomitantly, the Cyp19a1 expression and estrogen synthesis were significantly inhibited, which was validated i

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Li, Xun, Zhanwen Lin, Lei Wang, et al. "RNA-Seq Analyses of the Role of miR-21 in Acute Pancreatitis." Cellular Physiology and Biochemistry 51, no. 5 (2018): 2198–211. http://dx.doi.org/10.1159/000495866.

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Background/Aims: Our previous study demonstrated that a deficiency of microRNA 21 (miR-21) protects mice from acute pancreatitis, yet the underlying molecular networks associated with miR-21 in pancreatitis and pancreatitis-associated lung injury remain unexplored. Methods: We used next generation sequencing to analyze gene expression profiles of pancreatic tissues from wild-type (WT) and miR-21 knockout (KO) mice treated with caerulein by using a 1-day treatment protocol. The Database for Annotation, Visualization, and Integrated Discovery gene annotation tool and Ingenuity Pathway Analysis w

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Kee, Sydney Ann, Marcela T. Taruselli, John J. Ryan, and Amina Abdul Qayum. "MiR-146a is a negative regulator of IL-33-stimulated mouse mast cells." Journal of Immunology 202, no. 1_Supplement (2019): 185.5. http://dx.doi.org/10.4049/jimmunol.202.supp.185.5.

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Abstract Interleukin-33 (IL-33) is an inflammatory cytokine that promotes allergic disease by activating ILC2, Th2, and mast cells. IL-33 is increased in asthmatics, and its blockade suppresses asthma-like inflammation in mouse models. The IL-33 receptor, ST2, shares signaling cascades with the TLR family, but homeostatic control of ST2 function is poorly understood. MicroRNA-146a (miR-146a) is induced by LPS and suppresses TLR4 signaling in macrophages. Therefore, we explored whether miR-146a has a role in IL-33 signaling. IL-33 induced cellular and exosomal miR-146a expression in mouse bone

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Fedeli, Maya, Michela Riba, Jose Manuel Garcia Manteiga та ін. "miR-17∼92 family clusters control iNKT cell ontogenesis via modulation of TGF-β signaling". Proceedings of the National Academy of Sciences 113, № 51 (2016): E8286—E8295. http://dx.doi.org/10.1073/pnas.1612024114.

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Invariant natural killer T cells (iNKT) cells are T lymphocytes displaying innate effector functions, acquired through a distinct thymic developmental program regulated by microRNAs (miRNAs). Deleting miRNAs by Dicer ablation (Dicer KO) in thymocytes selectively impairs iNKT cell survival and functional differentiation. To unravel this miRNA-dependent program, we systemically identified transcripts that were differentially expressed between WT and Dicer KO iNKT cells at different differentiation stages and predicted to be targeted by the iNKT cell-specific miRNAs. TGF-β receptor II (TGF-βRII),

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Rahman, S., A. Elfiky, P. H. P. van Hamersveld, et al. "P032 MiR-511 deficiency aggravates T cell transfer colitis in mice." Journal of Crohn's and Colitis 15, Supplement_1 (2021): S147. http://dx.doi.org/10.1093/ecco-jcc/jjab076.161.

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Abstract Background MiR-511 is embedded in intron region 5 of the CD206/MRC1 gene, expressed by macrophage and dendritic cell populations. In this study, we aimed to investigate the effect of MiR-511 deficiency on intestinal inflammation in a murine T cell transfer colitis model. Methods A double MiR-511- and Rag-1 (knockout) KO mouse was generated and a T cell transfer colitis was induced by intraperitoneal injection of naïve T cells from donor WT mice. Since these mice lack mature T and B cells, first signs of inflammation appeared at week 3 after T cell injection. An endoscopy score was obt

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Graham, Natalie Marie, Wei-Le Wang, Estefany Reyes, and Mark P. Boldin. "The role of microRNA-142 in B cell activation and effector functions." Journal of Immunology 208, no. 1_Supplement (2022): 168.02. http://dx.doi.org/10.4049/jimmunol.208.supp.168.02.

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Abstract Control of gene expression by microRNA (miRNA) has recently emerged as a critical mechanism that regulates B cell activation and function. However, the role of specific miRNAs in this process is unclear. Using germline knockout (KO) mice, we have previously shown that miR-142 ablation impairs humoral immune responses despite significant expansion of the B cell compartment, suggesting that miR-142 is critical for B cell effector function and terminal differentiation. To more precisely dissect the role of miR 142 in B cell effector responses, we developed an activated B cell-specific mi

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Karaczyn, Aldona A., Edward Jachimowicz, Jaspreet S. Kohli, and Pradeep Sathyanarayana. "Loss of miR-199b Impairs Active Cycling of Hematopoietic Stem Cells during Steady-State Hematopoiesis." Blood 132, Supplement 1 (2018): 1283. http://dx.doi.org/10.1182/blood-2018-99-116381.

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Abstract Several recent studies have showed that dysregulation of microRNA (miRNA) expression in hematopoietic stem cells (HSC) can affect self-renewal of HSCs, and indicated a role for miRNAs in development of acute myeloid leukemia (AML). We and others have reported a significant down-regulation of miR-199b in AML patients. Recently we found that miR-199b is enriched in long-term hematopoietic stem cells (LT-HSC), suggesting that miR199-b may regulate HSCs function. Therefore, to understand the physiologic role of miR-199 in hematopoiesis during homeostasis, we evaluated various hematopoieti

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Xiong, Shuting, Jinsong Tian, Si Ge, et al. "The microRNA-200 cluster on chromosome 23 is required for oocyte maturation and ovulation in zebrafish†." Biology of Reproduction 103, no. 4 (2020): 769–78. http://dx.doi.org/10.1093/biolre/ioaa125.

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Abstract The reproductive process is usually controlled by the hypothalamic-pituitary-gonad axis in vertebrates, while Kiss/gonadotropin-releasing hormone (GnRH) system in the hypothalamus is required for mammalian reproduction but dispensable for fish reproduction. The regulation of follicle stimulating hormone/luteinizing hormone (LH) expression in fish species is still unknown. Here, we identified miR-200s on chromosome 23 (chr23-miR-200s) as important regulators for female zebrafish reproduction. Knockout of chr23-miR-200s (chr23-miR-200s-KO) resulted in dysregulated expression of luteiniz

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Li, Longlong, Yanling Zhu, Ting Chen, et al. "MiR-125b-2 Knockout in Testis Is Associated with Targeting to the PAP Gene, Mitochondrial Copy Number, and Impaired Sperm Quality." International Journal of Molecular Sciences 20, no. 1 (2019): 148. http://dx.doi.org/10.3390/ijms20010148.

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It has been reported that the miR-125 family plays an important role in regulating embryo development. However, the function of miR-125b-2 in spermatogenesis remains unknown. In this study, we used a model of miR-125b knockout (KO) mice to study the relationship between miR-125b-2 and spermatogenesis. Among the KO mice, the progeny test showed that the litter size decreased significantly (p = 0.0002) and the rate of non-parous females increased significantly from 10% to 38%. At the same time, the testosterone concentration increased significantly (p = 0.007), with a remarkable decrease for est

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Lu, Si-Yao, Chong-Lei Fu, Liang Liang, et al. "miR-218-2 regulates cognitive functions in the hippocampus through complement component 3–dependent modulation of synaptic vesicle release." Proceedings of the National Academy of Sciences 118, no. 14 (2021): e2021770118. http://dx.doi.org/10.1073/pnas.2021770118.

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microRNA-218 (miR-218) has been linked to several cognition related neurodegenerative and neuropsychiatric disorders. However, whether miR-218 plays a direct role in cognitive functions remains unknown. Here, using the miR-218 knockout (KO) mouse model and the sponge/overexpression approaches, we showed that miR-218-2 but not miR-218-1 could bidirectionally regulate the contextual and spatial memory in the mice. Furthermore, miR-218-2 deficiency induced deficits in the morphology and presynaptic neurotransmitter release in the hippocampus to impair the long term potentiation. Combining the RNA

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Xo'jaqulov, Azizjon, and Gulhayo Sayfullayeva. "QUYOSH ENERGIYASI - KELAJAK ENERGIYASI." Journal of Universal Science Research 1, no. 6 (2023): 555–57. https://doi.org/10.5281/zenodo.8042944.

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Biz kundalik hayotda ishlatadigan energiyaning deyarli 100 % i bu yoki boshqa tarzda o'zgartirilgan quyosh energiyasidir. Ko'mir - bu fotosintez orqali yashagan o'lik o'simliklar. Hatto o'tin yoqsangiz ham, siz o'tin yutgan quyosh energiyasini berasiz. Aslida, har qanday issiqlik elektr stantsiyasi ko'mir, neft, gaz va boshqa qazilmalar shaklida saqlanadigan quyosh energiyasini elektr energiyasiga aylantiradi.

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Bobomurodov, Azamat Yo'ldosh o'g'li. "SHARG'UN KO'MIR KONIDA QAZIB-YUKLASH ISHLARI TEXNIKASI VA TEXNOLOGIYASINING TAHLILI." RESEARCH AND EDUCATION 3, no. 5 (2024): 84–87. https://doi.org/10.5281/zenodo.11518018.

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<em>Mazkur</em><em> maqolada kon sanoati korxonalari faoliyatida </em><em>hamda jahonda Sharg‘un ko‘mir konida qazib – yuklash ishlari texnikasi va texnologiyasining taxlil qilish, ko‘mir qatlamlarini ekskavatorlar yordamida qazib – yuklash ishlarida yuqori unumdorlikka ega bo‘lgan ekskavatorlardan foydalanilgan va Karyerdagi qazib-yuklash ishlarining samaradorligini oshirish va kamchiliklarni bartaraf qilish</em><em> ishlari yoritib berilgan.</em>

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Jiang, Daifeng, та Ricardo Aguiar. "Microrna-155 Controls The RB/E2F Axis In Normal and Malignant B Cells Via The Non-Canonical TGFβ1-SMAD5 Signaling Module". Blood 122, № 21 (2013): 241. http://dx.doi.org/10.1182/blood.v122.21.241.241.

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Abstract MicroRNA-155 (miR-155) plays pleiotropic roles in the biology of normal and malignant B cells. MiR-155 knockout (KO) mice have fewer germinal center B cells, while overexpression of this miRNA is associated with aggressive DLBCL. Although several miR-155 targets have been identified, a mechanism that unifies the features of loss and gain of miR-155 function in normal and malignant cells remains to be described. In B cells, TGFβ signals are suppressive indicating that deregulation of this pathway may interfere with the developmental regulation of lymphocytes and contribute to the patho

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Flynn, Patrick A., and Evan Lind. "miR-146a −/− deficiency in the DC compartment results in increased effector phenotype CD4+ and CD8+ T cells in response to LCMV infection." Journal of Immunology 204, no. 1_Supplement (2020): 229.9. http://dx.doi.org/10.4049/jimmunol.204.supp.229.9.

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Abstract miR-146a is a micro-RNA that acts on transcripts upregulated in response to TLR induced signaling. Activation of TLRs results in maturation and survival of dendritic cells (DCs) to prime T cells. Interestingly, little is known how miR-146a regulates DC phenotype/function and whether it has direct effects on the regulation of T cell function. To probe this question, we utilized a miR-146a conditional knockout mouse model to study both DCs and lymphocytes. Our in vitro studies of DCs show that miR-146a KO BMDCs have increased uptake and processing of DQ-OVA, suggesting increased antigen

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Graham, Natalie Marie, Wei-Le Wang, Estefany Y. Reyes, and Mark P. Boldin. "The role of microRNA-142 in B cell activation and effector functions." Journal of Immunology 204, no. 1_Supplement (2020): 155.8. http://dx.doi.org/10.4049/jimmunol.204.supp.155.8.

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Abstract Control of gene expression by microRNA (miRNA) has recently emerged as a critical mechanism that regulates B cell activation and function. However, the role of specific miRNAs in this process is unclear. Using germline knockout (KO) mice, we have previously shown that miR-142 ablation impairs humoral immunity despite significant expansion of the B cell compartment, suggesting that miR-142 is critical for B cell effector function. We found that mice lacking miR-142 cannot generate specific antibody responses upon antigen challenge and display impaired germinal center (GC) formation and

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Wang, Huafeng, Bin Zhang, Wei-Le Wang, et al. "Downregulation of Mir-142 Promotes Leukemia Growth in Philadelphia Chromosome-Positive (Ph+) Acute Lymphoblastic Leukemia (ALL): A Possible Novel Therapeutic Target?" Blood 132, Supplement 1 (2018): 1338. http://dx.doi.org/10.1182/blood-2018-99-119599.

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Abstract The Philadelphia (Ph) chromosome or t(9;22) results in the generation of a fusion gene, namely BCR/ABL1, which encodes a chimeric protein with aberrant tyrosine kinase activity that drives leukemia cell growth and survival. This molecular/cytogenetic aberration occurs in ~20%-30% of ALL cases and confers poor prognosis. Ph+ ALL patients (pts) are often referred for allogeneic hematopoietic stem cell transplantation (alloHCT), although more recently BCR-ABL-specific tyrosine-kinase inhibitors (TKIs) and immunotherapeutic approaches seemingly induced long-term remission in some patients

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Martyniuk, Christopher J., Ruben Martínez, Daniel J. Kostyniuk, Jan A. Mennigen, and Jasenka Zubcevic. "Genetic ablation of bone marrow beta-adrenergic receptors in mice modulates miRNA-transcriptome networks of neuroinflammation in the paraventricular nucleus." Physiological Genomics 52, no. 4 (2020): 169–77. http://dx.doi.org/10.1152/physiolgenomics.00001.2020.

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Elucidating molecular pathways regulating neuroimmune communication is critical for therapeutic interventions in conditions characterized by overactive immune responses and dysfunctional autonomic nervous system. We generated a bone marrow-specific adrenergic beta 1 and beta 2 knockout mouse chimera (AdrB1.B2 KO) to determine how sympathetic drive to the bone affects transcripts and miRNAs in the hypothalamic paraventricular nucleus (PVN). This model has previously exhibited a dampened systemic immune response and decreased blood pressure compared with control animals. Reduced sympathetic resp

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X.A.Sattarov., Sattarov X.X. Anvarov A. Poʻlatova Sh. "O'G'IT SIFATIDA QO'NG'IR KO'MIRDAN SIFATIDA FOYDALANISH VA O'SIMLIKLARNI RIVOJLANISHIGA TA'SIRI." « Zamonaviy dunyoda tabiiy fanlar: Nazariy va amaliy izlanishlar» nomli ilmiy, masofaviy, onlayn konferensiyasi 1, no. 23 (2022): 42–44. https://doi.org/10.5281/zenodo.7131648.

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Tadqiqot ishida qo’ng’ir ko’mir mahsulotini ikki xil me’yori (2500, 5000 kg/ga) g’o’zaning o’sishi, rivojlanishiga ta’sirini o’rganildi. Olingan natijalar bo’yicha g’o’zaning gullash davri boshida tuproqda eng ko’p nitrat azoti  5000 kg/ga qo’ng’ir ko’mir mahsuloti solingan variantda aniqlandi va u tuproq xaydov qatlamida  (0-30 sm)-35,1 mg/kg ga teng. O’suv davrining ohirida ham bu variantda   N-NO3 miqdori-26,5 mg/kg ga tengligi aniqlandi.

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Zhang, Yue, Yifang Xie, Leifang Zhang, and Hang Zhao. "MicroRNA-155 Participates in Smoke-Inhalation-Induced Acute Lung Injury through Inhibition of SOCS-1." Molecules 25, no. 5 (2020): 1022. http://dx.doi.org/10.3390/molecules25051022.

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Smoke inhalation causes acute lung injury (ALI), a severe clinical disease with high mortality. Accumulating evidence indicates that microRNA-155 (miR-155) and suppressor of cytokine signaling 1 (SOCS-1), as mediators of inflammatory response, are involved in the pathogenesis of ALI. In this paper, we explored the proinflammatory mechanism of miR-155 in smoke-inhalation-induced ALI. Our data revealed that smoke inhalation induces miR-155 expression, and miR-155 knockout (KO) significantly ameliorates smoke-inhalation-induced lung injury in mice. Neutrophil infiltration and myeloperoxidase (MPO

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Kotani, Ai, Kazuki Okuyama, Bidisha Chanda, et al. "Mir-126 and Mir-195-Mediated Control of B Cell Fate in Leukemic and Normal Cells As a Potential Alternative for Transcriptional Factor." Blood 120, no. 21 (2012): 3533. http://dx.doi.org/10.1182/blood.v120.21.3533.3533.

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Abstract Abstract 3533 microRNAs (miRNAs) control many developmental and physiological processes. However, it is assumed to work as a fine tuner in cell fate determination, which has been shown to be regulated by transcription factors. Here, we challenge this canonical notion. miR-126 is downregulated in MLL-AF4 ALL, biphenotypic leukemia expressing both B cell and myeloid markers, compared with other types of ALLs. CD19 and CD20, B cell differentiation markers, were upregulated when miR-126 is reexpressed in MLL-AF4 ALLs (Figure 1). Interestingly, we found that miR-126, in leukemic cells, ind

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Wu, Yongxia, David Bastian, Jessica Lauren Heinrichs, et al. "Microrna-17-92 Cluster: Novel Target for Controlling Gvhd While Preserving GVL Effect." Blood 124, no. 21 (2014): 845. http://dx.doi.org/10.1182/blood.v124.21.845.845.

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Abstract Graft-versus-host disease (GVHD) remains a life threatening complication after allogeneic hematopoietic stem cell transplantation (HCT). Donor T cells are the key pathogenic effectors in the induction of GVHD. MicroRNAs (miRs) have been shown to play an important role in orchestrating immune response, among which miR-17-92 cluster is one of the best characterized miR clusters that encodes 6 miRs including 17, 18a, 19a, 20a, 19b-1 and 92-1. Although regulatory functions of miR-17-92 cluster have been elaborated in a variety of immune responses including anti-infection, anti-tumor, and

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Taruselli, Marcela T., Amina Abdul Qayum, and John J. Ryan. "MicroRNA-146a is a negative regulator of IL-33 stimulated mouse mast cells." Journal of Immunology 200, no. 1_Supplement (2018): 105.16. http://dx.doi.org/10.4049/jimmunol.200.supp.105.16.

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Abstract Interleukin 33 (IL-33) is an inflammatory cytokine that promotes allergic disease by activating ILC2, Th2 cells, and mast cells. IL-33 is increased in asthmatics, and its blockade suppresses asthma-like inflammation in mouse models. The IL-33 receptor, ST2, shares signaling cascades with the TLR family, but homeostatic control of ST2 function is poorly understood. MicroRNA-146a (miR-146a) is induced by LPS and suppresses TLR4 signaling in macrophages. Therefore, we explored whether miR-146a has a role in IL-33 signaling. IL-33 induced cellular and exosomal miR-146a expression in mouse

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He, Lishu, Jing Liu, Manoj Mishra, et al. "Abstract P127: microRNA-204 protects against Angiotensin II-induced apoptosis in podocytes via Sox4." Hypertension 81, Suppl_1 (2024). http://dx.doi.org/10.1161/hyp.81.suppl_1.p127.

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Background: We showed previously that global knockout (KO) of microRNA miR-204 attenuated hypertension but exacerbated renal injury including albuminuria in 14 days in C57BL/6J mice treated with uninephrectomy, angiotensin II, and a high-salt diet (Unx/AngII/salt). This suggests cell type-specific roles of miR-204. We hypothesize that miR-204 in podocytes protects against renal injury, specifically albuminuria via podocyte damage, in hypertension. Methods: We generated podocyte-specific miR-204 KO mice. Blood pressure and albuminuria were measured. RNA-seq in isolated miR-204 wild-type (WT) an

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Fujiwara, Yusuke, Chenyang Ding, Yohei Sanada, et al. "miR-23a/b clusters are not essential for the pathogenesis of osteoarthritis in mouse aging and post-traumatic models." Frontiers in Cell and Developmental Biology 10 (January 4, 2023). http://dx.doi.org/10.3389/fcell.2022.1043259.

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Osteoarthritis (OA), the most prevalent aging-related joint disease, is characterized by insufficient extracellular matrix synthesis and articular cartilage degradation and is caused by various risk factors including aging and traumatic injury. Most microRNAs (miRNAs) have been associated with pathogenesis of osteoarthritis (OA) using in vitro models. However, the role of many miRNAs in skeletal development and OA pathogenesis is uncharacterized in vivo using genetically modified mice. Here, we focused on miR-23–27–24 clusters. There are two paralogous miR-23–27–24 clusters: miR-23a-27a-24–2 (

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Zogg, Hannah, Rajan Singh, Se Eun Ha, et al. "miR‐10b‐5p rescues leaky gut linked with gastrointestinal dysmotility and diabetes." United European Gastroenterology Journal, September 18, 2023. http://dx.doi.org/10.1002/ueg2.12463.

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AbstractBackground/AimDiabetes has substantive co‐occurrence with disorders of gut‐brain interactions (DGBIs). The pathophysiological and molecular mechanisms linking diabetes and DGBIs are unclear. MicroRNAs (miRNAs) are key regulators of diabetes and gut dysmotility. We investigated whether impaired gut barrier function is regulated by a key miRNA, miR‐10b‐5p, linking diabetes and gut dysmotility.MethodsWe created a new mouse line using the Mb3Cas12a/Mb3Cpf1 endonuclease to delete mir‐10b globally. Loss of function studies in the mir‐10b knockout (KO) mice were conducted to characterize diab

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Hamed-Berair, Rihab E., Abhinav Agarwal, Marcin Wysoczynski, et al. "Abstract 19419: Anti Atherogenic Effects of Micro RNA - 21." Circulation 132, suppl_3 (2015). http://dx.doi.org/10.1161/circ.132.suppl_3.19419.

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Micro RNA-21 (miR-21), an evolutionary conserved micro RNA has been implicated in the pathogenesis of restenosis, myocardial infarction and heart failure. However, little is known about the role of miR-21 in atherosclerosis. Our data show that in vitro, LDL, oxidized LDL, acetylated LDL and LPS induced miR-21 by 2-3-fold (P<0.05) and down regulated its target protein PDCD4 in bone marrow derived macrophages (BMDM). Feeding the LDL receptor-knockout (LDLR-KO) mice with western diet (WD, 8-20 weeks) increased the abundance of miR-21 in BMDM by 1.5-fold (P<0.05). Basally, BMDM isolated from

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Zuo, Zhong, Han Lei, and Zhongjie Sun. "Abstract 9191: MicroRNA-150 is Essential in the Regulation of Blood Pressure." Circulation 124, suppl_21 (2011). http://dx.doi.org/10.1161/circ.124.suppl_21.a9191.

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Background & Hypothesis. Micro RNAs are small noncoding RNAs that regulate protein expression at the post-transcriptional level. The purpose of this study was to determine if microRNA-150 (miR-150) plays a role in the regulation of blood pressure (BP). Methods & Results. We found that knockout of miR-150 resulted in a significant increase in systolic, diastolic and mean BP in mice. Vascular relaxing responses to acetylcholine were decreased significantly in miR-150 knockout (miR150-KO) mice, suggesting impaired endothelial function. Therefore, miR-150 is essential in the maintenance of

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Semo, Jonathan, Gil Chernin, Michael Jonas, Sara Shimoni, and Jacob George. "Deletion of the Mir-106b~ 25 MicroRNA cluster attenuates atherosclerosis in Apolipoprotein E knockout mice." Lipids in Health and Disease 18, no. 1 (2019). http://dx.doi.org/10.1186/s12944-019-1155-8.

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Abstract Background MicroRNAs are short non-coding RNAs that regulate gene expression. The aim of this study was to gain an understanding of the possible role of the miR-106b~ 25 microRNA cluster in regulating atherosclerosis in mice. Methods MiR-106b~ 25 knockout mice were outcrossed into Apolipoprotein E (ApoE) knockout background to generate double knockout mice. At 36 weeks of age, lesion size was evaluated in the aortic sinus by oil-red-O staining. Results Lesion size was 2-fold smaller in double KO mice in comparison to ApoE KO mice. In addition, collagen staining showed a trend towards

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Esobi, Ikechukwu, Olanrewaju Oladosu, Jing Echesabal-Chen, Rhonda Powell, Terri Bruce, and Alexis D. Stamatikos. "Abstract 9535: The Effect of Vascular Smooth Muscle Cell miR-33a Expression on apoAI-Mediated Cholesterol Efflux and Macrophage-Like Cell Transdifferentiation." Circulation 146, Suppl_1 (2022). http://dx.doi.org/10.1161/circ.146.suppl_1.9535.

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Background: ABCA1 removes cellular cholesterol by participating in apoAI-mediated cholesterol efflux. MiR-33a is an SREBP-2 intronic miRNA that silences ABCA1, which impairs ABCA1-dependent cholesterol efflux. Thus, miR-33a expression may be atherogenic and previous data suggests inhibiting miR-33a in certain cells is atheroprotective. However, current data is scant on whether miR-33a expression in vascular smooth muscle cells (VSMC) is atherogenic. Moreover, cholesterol accumulation in VSMC results in these cells to transdifferentiate into an atherogenic macrophage-like cell (MLC). Therefore,

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Abduraxmanov, Davron Burxanjonovich. "QAZIB OLISH USULIDA MAHSULOT ISHLAB CHIQARUVCHI SANOAT KORXONALARINI ZAMONAVIY YONDASHUVLAR ASOSIDA MOLIYAVIY SOG'LOMLASHTIRISH YO'LLARI." April 23, 2025. https://doi.org/10.5281/zenodo.15269797.

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<em>Mazkur maqolada “O‘zbekko‘mir” AJ tarixi haqida qisqacha ma’lumot berilib, ko‘mir sanoati korxonalarini moliyaviy jihatdan sog‘lomlashtirish yo‘llari, birlamchi tahlil qilingan. Ko‘mir sanoatining istiqbolli rivojlanish yo‘nalishlari ko‘rsatib o‘tilgan shuningdek, xorijiy va mahalliy olimlarning fikrlaridan iqtiboslar keltirilib, muammoning nazariy va amaliy jihatlari o‘rganilgan.<strong> </strong></em>

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Colaianni, Davide, Federico Virga, Annamaria Tisi, et al. "miR-210 is essential to retinal homeostasis in fruit flies and mice." Biology Direct 19, no. 1 (2024). http://dx.doi.org/10.1186/s13062-024-00542-6.

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Abstract Background miR-210 is one of the most evolutionarily conserved microRNAs. It is known to be involved in several physiological and pathological processes, including response to hypoxia, angiogenesis, cardiovascular diseases and cancer. Recently, new roles of this microRNA are emerging in the context of eye and visual system homeostasis. Recent studies in Drosophila melanogaster unveiled that the absence of miR-210 leads to a progressive retinal degeneration characterized by the accumulation of lipid droplets and disruptions in lipid metabolism. However, the possible conservation of miR

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