- 遺伝子関連の、遺伝子関連性の
WordNet
- have or establish a relationship to; "She relates well to her peers"
- be in a relationship with; "How are these two observations related?" (同)interrelate
- give an account of; "The witness related the events"
- connected by kinship, common origin, or marriage
- being connected either logically or causally or by shared characteristics ; "painting and the related arts"; "school-related activities"; "related to micelle formation is the...ability of detergent actives to congregate at oil-water interfaces" (同)related to
- (genetics) a segment of DNA that is involved in producing a polypeptide chain; it can include regions preceding and following the coding DNA as well as introns between the exons; it is considered a unit of heredity; "genes were formerly called factors" (同)cistron, factor
- informal term for information; "give me the gen on your new line of computers"
PrepTutorEJDIC
- (…に)〈事件・事情など〉‘を'『物語る』《+『名』+『to』+『名』》 / (…と)…‘を'『関係させる』,結びつける《+『名』+『to(with)』+『名』》 / 〈物・事が〉(…に)関係がある,かかわる《+『to(with)』+『名(wh・節・句)』》 / (…に)〈人が〉なじむ,順応する《+『to』+『名』》
- 関係のある
- 遺伝子
UpToDate Contents
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- 1. 急性骨髄性白血病の予後 prognosis of acute myeloid leukemia
- 2. 急性骨髄性白血病の分子遺伝学 molecular genetics of acute myeloid leukemia
- 3. 成人における片頭痛の病態生理、臨床症状、および診断 pathophysiology clinical manifestations and diagnosis of migraine in adults
- 4. 原発性免疫不全症に対する遺伝子治療 gene therapy for primary immunodeficiency
- 5. 加齢黄斑変性：臨床像、病因、および診断 age related macular degeneration clinical presentation etiology and diagnosis
English Journal
- Birthdating of myenteric neuron subtypes in the small intestine of the mouse.
- Bergner AJ, Stamp LA, Gonsalvez DG, Allison MB, Olson DP, Myers MG Jr, Anderson CR, Young HM.Author information Department of Anatomy & Neuroscience, University of Melbourne, Victoria, Australia.AbstractThere are many different types of enteric neurons. Previous studies have identified the time at which some enteric neuron subtypes are born (exit the cell cycle) in the mouse, but the birthdates of some major enteric neuron subtypes are still incompletely characterized or unknown. We combined 5-ethynynl-2'-deoxyuridine (EdU) labeling with antibody markers that identify myenteric neuron subtypes to determine when neuron subtypes are born in the mouse small intestine. We found that different neurochemical classes of enteric neuron differed in their birthdates; serotonin neurons were born first with peak cell cycle exit at E11.5, followed by neurofilament-M neurons, calcitonin gene-related peptide neurons (peak cell cycle exit for both at embryonic day [E]12.5-E13.5), tyrosine hydroxylase neurons (E15.5), nitric oxide synthase 1 (NOS1) neurons (E15.5), and calretinin neurons (postnatal day [P]0). The vast majority of myenteric neurons had exited the cell cycle by P10. We did not observe any EdU+/NOS1+ myenteric neurons in the small intestine of adult mice following EdU injection at E10.5 or E11.5, which was unexpected, as previous studies have shown that NOS1 neurons are present in E11.5 mice. Studies using the proliferation marker Ki67 revealed that very few NOS1 neurons in the E11.5 and E12.5 gut were proliferating. However, Cre-lox-based genetic fate-mapping revealed a small subpopulation of myenteric neurons that appears to express NOS1 only transiently. Together, our results confirm a relationship between enteric neuron subtype and birthdate, and suggest that some enteric neurons exhibit neurochemical phenotypes during development that are different from their mature phenotype. J. Comp. Neurol. 522:514-527, 2014. © 2013 Wiley Periodicals, Inc.
- The Journal of comparative neurology.J Comp Neurol.2014 Feb 15;522(3):514-27. doi: 10.1002/cne.23423.
- There are many different types of enteric neurons. Previous studies have identified the time at which some enteric neuron subtypes are born (exit the cell cycle) in the mouse, but the birthdates of some major enteric neuron subtypes are still incompletely characterized or unknown. We combined 5-ethy
- PMID 23861145
- Expression profiles of genes involved in apoptosis and selenium metabolism in articular cartilage of patients with Kashin-Beck osteoarthritis.
- Wu SX1, Wang WZ2, Zhang F3, Wu CY3, Dennis BS3, Qu CJ4, Bai YD5, Guo X6.Author information 1Faculty of Public Health, College of Medicine of Xi'an Jiaotong University, Key Laboratory of Environment and Gene Related Diseases of Ministry Education, Key Laboratory of Trace Elements and Endemic Diseases, Ministry of Health, Xi'an 710061, China; Department of Orthopedics Surgery, The First Affiliated Hospital, College of Medicine of Xi'an Jiaotong University, Xi'an 710061, China.2Department of Orthopedics Surgery, The Second Affiliated Hospital, College of Medicine, Xi'an Jiaotong University, Xi'an 710004, China.3Faculty of Public Health, College of Medicine of Xi'an Jiaotong University, Key Laboratory of Environment and Gene Related Diseases of Ministry Education, Key Laboratory of Trace Elements and Endemic Diseases, Ministry of Health, Xi'an 710061, China.4Institute of Biomedicine, University of Eastern Finland, Kuopio, Finland; Biocenter Kuopio, University of Eastern Finland, Kuopio, Finland.5Department of Cellular and Structural Biology, University of Texas Health Sciences Center at San Antonio, 7703 Floyd Curl, San Antonio, TX 78229, USA.6Faculty of Public Health, College of Medicine of Xi'an Jiaotong University, Key Laboratory of Environment and Gene Related Diseases of Ministry Education, Key Laboratory of Trace Elements and Endemic Diseases, Ministry of Health, Xi'an 710061, China. Electronic address: Guox@mail.xjtu.edu.cn.AbstractKashin-Beck disease (KBD) is a special type of endemic osteoarthritis. It has been suggested that alterations in selenium metabolism and apoptosis play a role in KBD. However, the underlying molecular mechanism remains largely unclear. We performed a microarray analysis using RNA isolated from cartilages of KBD patients and healthy controls, through Significance Analysis of Microarray (SAM) software. Functional gene networks and crucial molecules associated with differentially expressed genes were investigated via Ingenuity Pathway Analysis (IPA) and hub gene analysis. Quantitative real-time PCR was used to check the validation of chip test. We identified 52 up-regulated apoptosis-related genes and 26 down-regulated selenium-related genes between KBD and controls, and these genes associated with the "MYC-mediated apoptosis signaling pathway". We confirmed the results from array studies with quantitative real-time PCR analysis. Our results suggest that abnormal regulation of selenium metabolism and apoptosis through the MYC mediated signaling pathway contributes to the pathogenesis of KBD, but the relationship between apoptosis gene and selenium gene was not found.
- Gene.Gene.2014 Feb 10;535(2):124-30. doi: 10.1016/j.gene.2013.11.050. Epub 2013 Dec 4.
- Kashin-Beck disease (KBD) is a special type of endemic osteoarthritis. It has been suggested that alterations in selenium metabolism and apoptosis play a role in KBD. However, the underlying molecular mechanism remains largely unclear. We performed a microarray analysis using RNA isolated from carti
- PMID 24316489
- Inflammation enhances Y1 receptor signaling, neuropeptide Y-mediated inhibition of hyperalgesia, and substance P release from primary afferent neurons.
- Taylor BK1, Fu W2, Kuphal KE3, Stiller CO4, Winter MK5, Chen W6, Corder GF2, Urban JH7, McCarson KE5, Marvizon JC6.Author information 1Department of Physiology, School of Medicine, University of Kentucky Medical Center, Lexington, KY 40536, USA. Electronic address: brad.taylor@uky.edu.2Department of Physiology, School of Medicine, University of Kentucky Medical Center, Lexington, KY 40536, USA.3Division of Pharmacology, University of Missouri-Kansas City, Kansas City, MO, USA.4Department of Medicine, Division of Clinical Pharmacology, Karolinska Hospital, Karolinska Institutet, Stockholm, Sweden.5Department of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, Kansas City, KS 66160, USA.6Veteran Affairs Greater Los Angeles Healthcare System and Division of Digestive Diseases, Department of Medicine, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, CA, USA.7Department of Physiology and Biophysics, The Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, IL, USA.AbstractNeuropeptide Y (NPY) is present in the superficial laminae of the dorsal horn and inhibits spinal nociceptive processing, but the mechanisms underlying its anti-hyperalgesic actions are unclear. We hypothesized that NPY acts at neuropeptide Y1 receptors in the dorsal horn to decrease nociception by inhibiting substance P (SP) release, and that these effects are enhanced by inflammation. To evaluate SP release, we used microdialysis and neurokinin 1 receptor (NK1R) internalization in rat. NPY decreased capsaicin-evoked SP-like immunoreactivity in the microdialysate of the dorsal horn. NPY also decreased non-noxious stimulus (paw brush)-evoked NK1R internalization (as well as mechanical hyperalgesia and mechanical and cold allodynia) after intraplantar injection of carrageenan. Similarly, in rat spinal cord slices with dorsal root attached, [Leu(31), Pro(34)]-NPY inhibited dorsal root stimulus-evoked NK1R internalization. In rat dorsal root ganglion neurons, Y1 receptors colocalized extensively with calcitonin gene-related peptide (CGRP). In dorsal horn neurons, Y1 receptors were extensively expressed and this may have masked the detection of terminal co-localization with CGRP or SP. To determine whether the pain inhibitory actions of Y1 receptors are enhanced by inflammation, we administered [Leu(31), Pro(34)]-NPY after intraplantar injection of complete Freund's adjuvant (CFA) in rat. We found that [Leu(31), Pro(34)]-NPY reduced paw clamp-induced NK1R internalization in CFA rats but not uninjured controls. To determine the contribution of increased Y1 receptor-G protein coupling, we measured [(35)S]GTPγS binding simulated by [Leu(31), Pro(34)]-NPY in mouse dorsal horn. CFA inflammation increased the affinity of Y1 receptor G-protein coupling. We conclude that Y1 receptors contribute to the anti-hyperalgesic effects of NPY by mediating the inhibition of SP release, and that Y1 receptor signaling in the dorsal horn is enhanced during inflammatory nociception.
- Neuroscience.Neuroscience.2014 Jan 3;256:178-94. doi: 10.1016/j.neuroscience.2013.10.054. Epub 2013 Oct 31.
- Neuropeptide Y (NPY) is present in the superficial laminae of the dorsal horn and inhibits spinal nociceptive processing, but the mechanisms underlying its anti-hyperalgesic actions are unclear. We hypothesized that NPY acts at neuropeptide Y1 receptors in the dorsal horn to decrease nociception by
- PMID 24184981
Japanese Journal
- Characterization of Perivascular Nerve Distribution in Rat Mesenteric Small Arteries
- Biological and Pharmaceutical Bulletin 38(11), 1757-1764, 2015
- NAID 130005106376
- T細胞アナジーとE3ユビキチンリガーゼ
- 臨床免疫・アレルギー科 62(4), 411-417, 2014-10
- NAID 40020239442
- 1P-016 出芽酵母高温耐性関連遺伝子の分離と分子育種による耐性強化(遺伝子工学,一般講演)
- 日本生物工学会大会講演要旨集 66, 21, 2014-08-05
- NAID 110009906097
Related Links
- Calcitonin gene related peptide (CGRP) is a member of the calcitonin family of peptides, which in humans exists in two forms, α-CGRP and β-CGRP. α-CGRP is a 37-amino acid peptide and is formed from the alternative splicing of ...
- (genetics) gene Related terms [edit] genetica genetico genetista genico genotipo Middle Dutch [edit] Alternative forms [edit] ghene Etymology [edit] From Old Dutch *gēn, from Proto-Germanic *jainaz. Pronunciation [edit] IPA (key) ...
Related Pictures
★リンクテーブル★
| リンク元 | 「遺伝子関連」「遺伝子関連性」 |
| 拡張検索 | 「calcitonin gene-related peptide receptor」「calcitonin gene-related peptide」 |
| 関連記事 | 「relate」 |
「遺伝子関連」
- 英
- gene-related
- 関
- 遺伝子関連性
「遺伝子関連性」
- 英
- gene-related
- 関
- 遺伝子関連
「relate」
- v.
- 関連する、関係する
- 関
- associate、association、attach、bearing、concern、connect、connection、correlate、correlation、germane、implicate、implication、interplay、link、pertain、pertinent、referable、reference、relation、relationship、relative、relevance、relevant、respect