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胚胎基因活性维持至成年状态。

Maintenance of embryonic gene activity into the adult state.

作者信息

Hancock R L

机构信息

Canadian Institute of Theoretical Biology, Nova Scotia.

出版信息

Med Hypotheses. 1992 Apr;37(4):250-4. doi: 10.1016/0306-9877(92)90196-j.

DOI:10.1016/0306-9877(92)90196-j
PMID:1625602
Abstract

It is now apparent that certain embryonic gene activities may be maintained before the transition from embryonic to the adult state takes place. The consequence of such a condition could have far reaching results and create a totally new approach to biotechnology by dealing with epigenetic methods and not gene-splicing methods. For example, if a group of c-oncogenes, believed to be of the embryonic type (1) that are responsible for growth factors which regulate embryonic rates of growth, then large increases in growth rates during the adult stage should occur. Two major alterations seem to be required. One is the interference of DNA methylation patterns using such agents as ethionine (interfering with S-adenoysl-1-methionine synthesis) or azacytidine (interfering with DNA methylase activity). Secondly, a change in chromatin configuration (deheterochromatization?) with agents such as n-butyrate or hexamethylenebisacetamide (HMBA). Maintenance methylases would make the altered (hypomethylated) pattern of the perturbed chromatin invariant after the initial perturbation. Enhancer-promoter mechanics are probably pertinent to this process.

摘要

现在很明显,某些胚胎基因活动可能在从胚胎状态向成年状态转变之前就得以维持。这种情况的后果可能会产生深远影响,并通过处理表观遗传方法而非基因拼接方法,为生物技术创造一种全新的途径。例如,如果一组被认为是胚胎类型的原癌基因(1)负责调控胚胎生长速率的生长因子,那么在成年阶段生长速率应该会大幅提高。似乎需要进行两项主要改变。一是使用诸如乙硫氨酸(干扰S - 腺苷 - 1 - 甲硫氨酸合成)或氮杂胞苷(干扰DNA甲基化酶活性)等试剂来干扰DNA甲基化模式。其次,使用诸如丁酸盐或六亚甲基双乙酰胺(HMBA)等试剂来改变染色质构型(去异染色质化?)。维持甲基化酶会使初始扰动后受干扰染色质的改变(低甲基化)模式保持不变。增强子 - 启动子机制可能与这个过程相关。

相似文献

1
Maintenance of embryonic gene activity into the adult state.胚胎基因活性维持至成年状态。
Med Hypotheses. 1992 Apr;37(4):250-4. doi: 10.1016/0306-9877(92)90196-j.
2
Generalizing the control process for embryonic genes.概括胚胎基因的控制过程。
Med Hypotheses. 1992 Apr;37(4):245-9. doi: 10.1016/0306-9877(92)90195-i.
3
Theoretical mechanisms for synthesis of carcinogen-induced embryonic proteins: XXIII. Enhancer theory.致癌物诱导胚胎蛋白合成的理论机制:XXIII. 增强子理论。
Med Hypotheses. 1989 Nov;30(3):187-94. doi: 10.1016/0306-9877(89)90060-1.
4
A specific mechanism for ethionine-induced embryonic gene activity.乙硫氨酸诱导胚胎基因活性的特定机制。
Med Hypotheses. 1993 May;40(5):284-6. doi: 10.1016/0306-9877(93)90007-d.
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Biochemical formulations of embryonic gene control.胚胎基因控制的生化制剂。
Med Hypotheses. 1993 May;40(5):287-95. doi: 10.1016/0306-9877(93)90008-e.
6
Theoretical mechanisms for synthesis of carcinogen-induced embryonic proteins: intermediate generalizations.致癌物诱导胚胎蛋白合成的理论机制:中间概括
Med Hypotheses. 1991 Sep;36(1):65-8. doi: 10.1016/0306-9877(91)90165-u.
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Theoretical mechanisms for synthesis of carcinogen-induced embryonic proteins: XII mutational and non-mutational mechanism as subsets of a more general mechanism. Part A--Ethionine.
Med Hypotheses. 1984 Nov;15(3):323-31. doi: 10.1016/0306-9877(84)90022-7.
8
Theoretical mechanisms for synthesis of carcinogen-induced embryonic protein: XXI. Oncogenes interpreted as embryonic genes.致癌物诱导胚胎蛋白合成的理论机制: XXI. 癌基因被解释为胚胎基因。
Med Hypotheses. 1988 Oct;27(2):93-7. doi: 10.1016/0306-9877(88)90153-3.
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Theoretical mechanisms for synthesis of carcinogen-induced embryonic proteins: XV. Preliminary generalizations.致癌物诱导胚胎蛋白合成的理论机制:XV. 初步归纳。
Med Hypotheses. 1986 Apr;19(4):403-12. doi: 10.1016/0306-9877(86)90116-7.
10
Theoretical mechanisms for synthesis of carcinogen-induced embryonic proteins: XXIV. Repeated embryonic genes in liver.致癌物诱导胚胎蛋白合成的理论机制:XXIV. 肝脏中的重复胚胎基因。
Med Hypotheses. 1991 Mar;34(3):256-60. doi: 10.1016/0306-9877(91)90220-s.