MYC（8q24）基因斷裂探針

 廣州健侖生物科技?有限公司 

本司長期供應(yīng)尼古丁（可替寧）檢測試劑盒，其主要品牌包括美國NovaBios、廣州健侖、廣州創(chuàng)侖等進(jìn)口產(chǎn)品，國產(chǎn)產(chǎn)品，試劑盒的實(shí)驗(yàn)方法是膠體金方法。

我司還有很多熒光原位雜交系列檢測試劑盒以及各種FISH基因探針和染色體探針等，。

MYC（8q24）基因斷裂探針

   本試劑盒主要用于MYC（8q24）基因斷裂的檢測，里面包括即用型雜交液和DAPI復(fù)染劑。
本試劑盒僅供科研使用。

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二維碼掃一掃

【公司名稱】 廣州健侖生物科技有限公司
【】    楊永漢 

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【騰訊 】
【公司地址】 廣州清華科技園創(chuàng)新基地番禺石樓鎮(zhèn)創(chuàng)啟路63號二期2幢101-3室

【企業(yè)文化宣傳】

生殖細(xì)胞負(fù)責(zé)遺傳信息的時(shí)代傳遞，那么基因組的完整性對于生殖細(xì)胞至關(guān)重要。而在真核生物精細(xì)胞中，有許多外來侵入的轉(zhuǎn)座子、逆轉(zhuǎn)座子等移動(dòng)型遺傳元件。這些自私的遺傳元件在染色體不同位點(diǎn)間跳躍，造成基因突變和基因組損傷。在生殖細(xì)胞中，轉(zhuǎn)座子的跳躍可能會(huì)導(dǎo)致不育。PiRNA/Piwi能夠高效的阻止轉(zhuǎn)座子等元件對基因組的損傷。研究發(fā)現(xiàn)，piRNA起源于反轉(zhuǎn)座子、重復(fù)序列等區(qū)域，與Piwi蛋白形成piRNA/Piwi機(jī)器，沉默轉(zhuǎn)座子、反轉(zhuǎn)座子等。此外，piRNA還可以發(fā)揮類似于siRNA的功能，參與調(diào)控生殖細(xì)胞中編碼基因的表達(dá)。

方法：

研究人員發(fā)現(xiàn)無精子癥患者體內(nèi)Piwi（Hiwi）生殖突變會(huì)阻止其泛素化和降解。為了了解其中的作用機(jī)制，研究人員構(gòu)建了Piwi（Miwi）突變敲入小鼠模型，證明了這種遺傳缺陷直接導(dǎo)致了男性不育癥。具體來說，研究人員發(fā)現(xiàn)MIWI能以一種對立于Piwi作用RNA（piRNA）的方式，與組蛋白泛素連接酶RNF8結(jié)合，并在晚期精子細(xì)胞的細(xì)胞質(zhì)中穩(wěn)定螯合RNF8，從而導(dǎo)致精子異常，引起組蛋白滯留，形態(tài)異常和活性嚴(yán)重受損，而這可以通過RNF8-N阻斷精子細(xì)胞中RNF8-MIWI的相互作用，逆轉(zhuǎn)功能。

結(jié)果1：

研究人員篩查了413例臨床無精、弱精癥患者Piwi基因上控制Piwi蛋白泛素化修飾降解的關(guān)鍵元件D-box，發(fā)現(xiàn)有3例病人在此元件中存在雜合性基因突變，且發(fā)現(xiàn)此類突變可來源于基因自發(fā)突變，也可從母親遺傳獲得。為鑒定此類突變是否是造成這些患者發(fā)生無精/少弱精的原因，研究人員將其中的一組突變條件型敲入小鼠Piwi基因，在小鼠模型中研究此類突變對精子發(fā)生的作用。他們發(fā)現(xiàn)， Piwi D-box雜合突變小鼠均出現(xiàn)雄性不育，精子表型也與患者*。深入研究發(fā)現(xiàn)，Miwi D-box雜合突變小鼠精子發(fā)生阻滯在延長型精子細(xì)胞發(fā)育階段，盡管能產(chǎn)生少量精子，但精子形態(tài)異常、細(xì)胞核結(jié)構(gòu)疏松、無活力。

結(jié)果2：

機(jī)制研究揭示， PIWI蛋白具有將RNF8“扣留”于細(xì)胞核外的功能。正常小鼠體內(nèi)PIWI蛋白會(huì)在精子發(fā)育后期被自然降解，RNF8進(jìn)入細(xì)胞核內(nèi)開啟“組蛋白-魚精蛋白轉(zhuǎn)換”，幫助精子發(fā)育完成。而Piwi蛋白突變導(dǎo)致其在后期不能被正常代謝，大量RNF8因此被“扣留”在細(xì)胞核外，魚精蛋白與組蛋白交換受阻，zui終造成精子發(fā)育受阻。將RNF8-N端導(dǎo)入突變小鼠的精子細(xì)胞后，可有效阻斷Piwi基因蛋白產(chǎn)物對RNF8的“扣留”，恢復(fù)精子的正常形態(tài)及游動(dòng)能力，提示該策略對臨床治療此類無精、弱精癥具有重要理論參考價(jià)值。

Reproductive cells are responsible for the transmission of genetic information, then the integrity of the genome is crucial to the germ cells. In eukaryote, there are many intruded transposons, reverse transposons, and other genetic elements. These selfish genetic elements jump between chromosomal locations, causing gene mutations and genome damage. In the germ cells, the leaping of the transposon may lead to infertility. PiRNA/Piwi can effectively prevent the damage to the genome by the components of the transposon. It is found that piRNA originates in the retrotransposon, repeat sequence and other regions, and forms the piRNA/Piwi machine with the Piwi protein, silencing the transposon, and the retrotransposon. In addition, piRNA can also play a role similar to siRNA and participate in the regulation of the expression of encoded genes in the germ cells.

Method：

The researchers found that Piwi (Hiwi) mutagenesis in the body of azoospermia prevents its ubiquitination and degradation. In order to understand the mechanism, the researchers constructed a Piwi (Miwi) in mouse model of mutation, proved the genetic defects directly lead to male infertility. Specifically, the researchers found that MIWI in a Piwi RNA (piRNA) in the way of combination with histone RNF8 ubiquitin ligase, and stable chelate RNF8 in advanced sperm cell cytoplasm, resulting in abnormal sperm, cause protein retention, abnormal morphology and activity severely damaged, this can be done by RNF8-N blocking the interaction of RNF8-MIWI in sperm cells, reverse function.

Results 1:

The key element of D-box researchers screened 413 cases of azoospermia and weak sperm Piwi in patients with Piwi gene controlling protein ubiquitination and degradation, discovered the existence of heterozygous mutations in 3 patients in this element, and found that these mutations can be derived from spontaneous mutation gene can be inherited from his mother. For the identification of such mutations is the cause of azoospermia / little weak sperm occurred in these patients, the researchers will be a group of mutant type Piwi gene knock in mouse condition which, in a mouse model of such mutations on spermatogenesis function. They found that the Piwi D-box heterozygous mutant mice were male sterility, and the sperm phenotype was also consistent with the patient. Further studies showed that Miwi D-box heterozygous mutant mice had spermatogenesis arrest at the extended stage of spermatogenesis, although they produced a small amount of sperm, but the sperm morphology was abnormal, the nuclear structure was loose and inactive.

Results 2:

The mechanism studies have revealed that PIWI protein has the function of "withholding" RNF8 outside the nucleus. In normal mice, PIWI protein will be degraded naturally in the late stage of sperm development. RNF8 will enter into the nucleus and start the histone protamine transformation to help sperm development. However, the mutation of Piwi protein causes it to not be metabolize in the late stage. A large number of RNF8 is therefore "arrested" outside the nucleus. The exchange of protamine and histone is hindered, resulting in the development of sperm is blocked. After introducing the RNF8-N terminal into the spermatozoa of the mutant mice, it can effectively block the retention of Piwi protein products to RNF8 and restore the normal morphology and swimming ability of the sperm, suggesting that this strategy has important theoretical reference value for the clinical treatment of such azoospermia and asthenospermia.