子宫内膜癌中磷脂酰肌醇3激酶/蛋白激酶通路活化及临床意义

目的 探讨磷脂酰肌醇3激酶/蛋白激酶( PI3 K/AKT)信号通路的重要组分PTEN、PIK3CA和p-AKT在子宫内膜癌组织中的改变及其预后意义.方法 免疫组织化学EnVision二步法检测PTEN、p-AKT、雌激素受体(ER)和孕激素受体在71例子宫内膜癌组织中的表达,聚合酶链反应测序法分析其中34例PIK3CA基因外显子9和20的突变情况.结果 (1)71例子宫内膜癌组织中,子宫内膜样癌( EEC) 65例,非子宫内膜样癌(NEEC)6例.PTEN失表达率为63.4％( 45/71),在EEC中的比例(66.2％,43/65)高于NEEC( 2/6;P=0.18).PTEN失表达患者(45例)预后优于PTEN正常表达者(26例;P=0.07).进一步分组分析显示在ER阴性病例中,PTEN失表达者(12例)的预后优于PTEN正常表达者(7例),差异有统计学意义(P=0.04).(2)本组34例中PIK3CA突变率为41.2％ (14/34),突变热点为外显子9的T544.PIK3CA突变在EEC中的发生比例(44.8％,13/29)高于NEEC( 1/5;P ＞0.05).外显子9突变全部见于Ⅰ期EEC病例中,且在高、中分化的EEC中发生率高于低分化肿瘤(P＞0.05).外显子20突变在早期病例组(14.3％,4/28)的发生率显著低于晚期病例组(4/6;P=0.0l).(3)p-AKT的阳性率为59.2％ (42/71),在EEC中的阳性率(60.0％,39/65)高于NEEC(3/6;P=0.68);但高、中分化组EEC的阳性比例(75.0％,21/28;53.6％,15/28)高于低分化组(3/9),差异有统计学意义(P=0.02).p-AKT阳性与ER阳性相关(r=0.339,P=0.00).结论 PI3K/AKT信号通路的关键分子,如PTEN失表达、p-AKT阳性提示预后好.PIK3CA基因外显子9和20的突变对子宫内膜癌的预后影响可能不同.子宫内膜癌中PTEN和p-AKT的功能可能受到ER状态的影响.     

氧化苦参碱改善高脂诱导ApoE~(-/-)小鼠的胰岛素抵抗

目的:观察氧化苦参碱对高脂诱导胰岛素抵抗小鼠的作用并初步探讨可能机制。方法:Apo E~(-/-)小鼠高脂喂养16周,分为胰岛素抵抗组以及氧化苦参碱25、50、100 mg/kg组,C57BL/6J小鼠设为对照组,每组10只。灌胃给药8周后,进行小鼠葡萄糖耐量实验;测定血清空腹血糖(FBG)、甘油三酯(TG)、胆固醇(TC)、游离脂肪酸(FFA)和空腹胰岛素(FINS)的含量;实时荧光定量PCR测定肝组织胰岛素受体(INSR)、胰岛素受体底物-2(IRS-2)和葡萄糖转运子2(GLUT_2)的mRNA表达;Western blot法测定肝组织GLUT_2、INSR、IRS-2、p-INSR、p-IRS-2、磷脂酰肌醇3-激酶(PI3K)、p-PI3K、丝氨酸/苏氨酸蛋白激酶(AKT)和p-AKT的蛋白水平。结果:氧化苦参碱能不同程度降低FBG、TG、TC、FFA和FINS水平,改善胰岛素抵抗;氧化苦参碱组INSR、IRS-2和GLUT_2的mRNA表达比胰岛素抵抗组升高(P0.05),p-INSR/INSR、p-IRS-2/IRS-2、p-PI3K/PI3K、p-AKT/AKT和GLUT_2的蛋白水平也升高(P0.05)。结论:氧化苦参碱能通过PI3K/AKT通路,改善高脂诱导小鼠的胰岛素抵抗。     

多囊卵巢综合征胰岛素抵抗患者Gly972Arg多态性与子宫内膜胰岛素受体底物1表达的关系

目的:研究多囊卵巢综合征(Polycystic ovary syndrome,PCOS)胰岛素抵抗(Insulin resistance,IR)患者胰岛素受体底物1(Insulin receptor substrate,IRS-1)基因Gly972Arg多态性与子宫内膜IRS-1表达的关系。方法:PCOS患者51例,用聚合酶链反应(PCR)技术,检测IRS-1Gly972Arg多态性。于月经周期第1天刮取子宫内膜,合并胰岛素抵抗者28例,非胰岛素抵抗者23例,应用免疫组化技术检测子宫内膜IRS-1,计算机图像分析系统分析子宫内膜IRS-1的表达。结果:Gly972Arg多态性:51例PCOS患者中,基因型GG 49例,基因型GA 2例,IR组与无IR组各1例,两组比较无统计学意义。子宫内膜IRS-1的表达:IR组、非IR组IRS-1表达的灰度值分别为131.94±18.39、78.16±6.87,比较有统计学意义(P<0.01)。结论:IRS-1Gly972Arg的突变率较低,其多态性在PCOS IR组与无IR组比较无统计学意义(P>0.05),不影响子宫内膜IRS-1的表达。     

糖尿病大鼠肺组织PI3K/Akt表达的变化及意义

目的研究糖尿病大鼠肺组织磷脂酰肌醇3激酶(PI3K)/丝氨酸-苏氨酸激酶(Akt)表达的变化及意义。方法 40只大鼠随机分为对照组(10)和糖尿病组(30),通过高糖、高脂饮食加腹腔注射小剂量链脲佐菌素(STZ)的方法建立2型糖尿病大鼠模型。糖尿病模型建立后,检测血糖、血脂的改变;采用免疫组织化学方法和Western blot方法检测各组大鼠肺组织中PI3K、Akt和p-Akt表达的变化情况。结果与对照组比较,糖尿病模型组大鼠血糖、血脂值明显增高(0.01)。免疫组织化学和Western blot结果显示,糖尿病模型组大鼠模肺组织PI3K、Akt和pAkt的表达量均显著高于对照组。结论 PI3K/Akt信号通路可能参了与糖尿病肺组织病变的发生发展。     

瑞舒伐他汀通过抑制PI3K/AKT信号通路活性缓解小鼠颈动脉粥样硬化

目的探讨瑞舒伐他汀缓解小鼠颈动脉粥样硬化的机制及相关信号通路。方法将75只Apo E-/-小鼠随机分为5组,采取不同的干预措施,分别为对照组、颈动脉粥样硬化模型组、瑞舒伐他汀低剂量组、中剂量组、高剂量组。检测5组小鼠的血脂相关指标;实验结束后,处死小鼠,采用PCR技术,检测各组小鼠颈动脉组织中MMP-2 mRNA、MMP-9 mRNA的表达差异;采用Western-blot检测颈动脉组织中p-PI3K蛋白、p-AKT蛋白、PI3K蛋白、AKT蛋白的表达水平。结果①与模型组相比,3个瑞舒伐他汀治疗组小鼠的TC、TG、LDL-C水平明显下降,HDL-C明显升高(P0.05)。3个治疗组小鼠颈动脉总面积与模型组相比差异无统计学意义(P0.05),但斑块面积显著较小(P0.05),且高剂量组的斑块面积最小。②对照组小鼠颈动脉组织中MMP-2的阳性率较低,模型组的MMP-2的阳性率及染色强度明显较高。低、中、高剂量组的的染色阳性率及染色强度较模型组有明显下降。③模型组小鼠颈动脉组织中MMP-2 mRNA、MMP-9 mRNA的相对表达量显著最高,低剂量组次之,高剂量组表达水平最低。Western-blot检测结果趋势与RT-PCR一致。④与对照组相比,模型组小鼠颈动脉组织中p-PI3K蛋白、p-AKT蛋白表达量明显升高(P0.05)。与模型组比较,瑞舒伐他汀3个治疗组的小鼠颈动脉组织中p-PI3K蛋白、p-AKT蛋白表达量逐渐下降。结论瑞舒伐他汀可通过抑制PI3K/AKT信号通路活性对颈动脉粥样硬化小鼠发挥保护作用。     

METTL14通过PI3K/AKT/GSK3β/β-catenin信号通路调控巨噬细胞分化对宫颈癌细胞凋亡和增殖的影响北大核心CSCD

目的探讨METTL14通过调控巨噬细胞分化抑制宫颈癌病理性发展及相关机制。方法检测宫颈癌病变样本METTL14 m RNA和蛋白,以及IL-6、iNOS、Arg-1和CD206表达变化。PMA诱导THP-1细胞转化为巨噬细胞,慢病毒过表达或抑制METTL14表达,检测IL-6、iNO、Arg-1和CD206表达变化以及PI3K/AKT/GSK3β/β-catenin信号通路相关蛋白表达情况。随后加入PI3K/AKT/GSK3β/β-catenin信号通路激动剂和抑制剂,检测过表达或抑制METTL14后,巨噬细胞IL-6、iNO、Arg-1和CD206表达变化,并取其上清制成条件培养基,孵育Hela细胞,检测细胞凋亡和增殖情况。结果1)宫颈癌病变组织中METTL14 mRNA和蛋白表达降低(P<0.05),巨噬细胞M1型标志物IL-6和iNOS表达明显降低(P<0.05),而M2型标志物Arg-1和CD206表达明显升高(P<0.05)。2)巨噬细胞过表达METTL14后,IL-6和iNOS表达明显升高(P<0.05),而Arg-1和CD206表达明显降低(P<0.05),M1/M2比例升高;抑制METTL14表达后,M1型标志物降低(P<0.05),M2型标志物升高(P<0.05),M1/M2比例降低。3)巨噬细胞中转染OE-METTL14慢病毒组PI3K/AKT/GSK3β/β-catenin信号通路被抑制(P<0.05);加入PI3K/AKT激动剂后,M1型标志物降低而M2型标记物升高(P<0.05),M1/M2比例降低;OE-METTL14可逆转此趋势。Sh-METTL14慢病毒组PI3K/AKT/GSK3β/β-catenin信号通路被激活(P<0.05),加入PI3K/AKT抑制剂后,M1型标志物升高而M2型标记物降低(P<0.05),M1/M2比例升高;Sh-METTL14可逆转此趋势。4)取转染OE-METTL14慢病毒后的巨噬细胞上清培养Hela细胞,可见细胞凋亡明显增多(P<0.05),增殖明显减少(P<0.05)。Sh-METTL14组的Hela细胞则表现出细胞凋亡减少(P<0.05),增殖增多(P<0.05)。结论METTL14通过PI3K/AKT/GSK3β/β-catenin信号通路调控巨噬细胞分化可能有促进宫颈癌细胞凋亡,抑制增殖的作用。     

子宫内膜异位症中组蛋白H3K27Me3及其修饰酶的表达及意义

目的探讨组蛋白H3K27Me3及其修饰酶EZH2、KDM6B在子宫内膜异位症(endometriosis, EM)中的表达及意义。方法收集30例腹腔镜下手术切除卵巢EM病灶组织(增生期和分泌期各15例)及30例其它异位部位EM病灶组织(8例结直肠、10例盆腔、7例腹壁皮肤、5例输卵管)为实验组,60例因子宫肌瘤或卵巢纤维瘤等良性病变行在位子宫内膜诊刮组织为对照组(增生期和分泌期各30例)。采用免疫组化EnVision两步法及Western blot法检测H3K27Me3、EZH2、KDM6B的表达水平。收集实验组卵巢EM的临床各指标,包括患者年龄、体重指数(BMI)、病灶大小、痛经评分、月经周期、盆腔液CA125浓度、rAFS评分,应用相应统计学方法分析H3K27Me3及其修饰酶的表达与临床各指标的相关性。结果 H3K27Me3和EZH2在实验组卵巢EM病灶与对照组正常分泌期子宫内膜中的表达差异无显著性(P0.05),两者的表达水平均高于对照组正常增生期子宫内膜(P0.01),KDM6B在各组中均高表达且组间差异无显著性(P0.05);各蛋白在实验组不同异位部位中的表达差异无显著性(P0.05);月经周期对卵巢EM组各蛋白的表达无显著影响(P0.05)。患者年龄、BMI、病灶大小、盆腔液CA125浓度及rAFS评分与H3K27Me3、EZH2的表达呈正相关(P0.01),痛经程度与H3K27Me3、EZH2的表达无相关性(P0.01)。结论组蛋白H3K27Me3及其修饰酶EZH2在EM中高表达,孕酮可通过EZH2的甲基化作用使H3K27Me3的表达增加。H3K27Me3、EZH2的表达水平可在一定程度上反映EM病变严重程度,H3K27Me3可能成为EM的一个潜在生物蛋白标记,EZH2作为H3K27Me3的修饰酶或能成为EM诊治的潜在新靶点。     

Asprosin、CTRP3在多囊卵巢综合征患者血清中的表达及其临床意义

目的 探讨白脂素(Asprosin)、C1q肿瘤坏死因子相关蛋白3(CTRP3)在多囊卵巢综合征(PCOS)患者血清中的表达及其与相关生化指标的相关性.方法 选取2019年6月至2021年3月期间在我院接受治疗的初诊PCOS患者92例作为PCOS组,根据胰岛素抵抗指数(HOMA-IR)将其分为非IR组和IR组,另根据体质量指数(BMI)将其分为体重正常组和超重组.另选取同期在我院体检的健康孕龄女性50例作为对照组.采用酶联免疫吸附法检测血清Asprosin、CTRP3的水平,另收集所有研究对象的糖脂代谢指标和性激素指标.结果 PCOS组的BMI、总胆固醇、低密度脂蛋白胆固醇(LDL-C)、三酰甘油、空腹胰岛素、空腹血糖、HOMA-IR、促黄体生成素(LH)、催乳素、Asprosin水平均高于对照组,CTRP3水平低于对照组(P<0.05).IR组的BMI、三酰甘油、空腹胰岛素、空腹血糖、Asprosin水平均高于非IR组,CTRP3水平低于非IR组(P<0.05).超重组的总胆固醇、三酰甘油、空腹胰岛素、空腹血糖、HOMA-IR、Asprosin水平均高于体重正常组,CTRP3水平低于体重正常组(P<0.05).PCOS患者血清Asprosin与BMI、总胆固醇、三酰甘油、空腹胰岛素、空腹血糖、HOMA-IR、LH呈正相关,与CTRP3呈负相关(P<0.05);PCOS患者血清CTRP3与BMI、三酰甘油、空腹胰岛素、空腹血糖、HOMA-IR、Asprosin呈负相关(P<0.05).结论 Asprosin在多囊卵巢综合征患者血清中异常高表达,CTRP3异常低表达,二者的表达水平与患者的IR程度和肥胖情况密切相关.     

PI3K/Akt在多囊卵巢综合征发病机制中作用的研究进展

多囊卵巢综合征(PCOS)是一种生殖功能障碍合并代谢障碍的内分泌疾病,其病因及发病机制尚未明确。磷酯酰肌醇-3激酶/蛋白激酶B(PI3K/Akt)信号通路中的信号分子及蛋白的改变与PCOS患者胰岛素抵抗的发生、脂肪细胞的分化、细胞增殖及治疗预后有关。     

磷脂酰肌醇3激酶促进支气管哮喘大鼠气道平滑肌细胞增殖

目的探讨磷脂酰肌醇3激酶(PI3K)在支气管哮喘大鼠气道重构中的作用。方法将24只SD大鼠随机分为3组:正常对照组,哮喘4周组和6周组,每组8只。测定气道反应性并观察气道壁嗜酸性粒细胞的浸润情况;图像分析软件测定支气管壁厚度、支气管平滑肌厚度及支气管平滑肌细胞核数量;用免疫组织化学染色方法检测PI3K蛋白表达;逆转录聚合酶链反应(RT-PCR)检测PI3KmRNA表达。结果PI3K P85α主要在气道上皮细胞、气道平滑肌细胞表达。哮喘4周和6周组PI3K P85α蛋白及mRNA表达显著高于对照组(P<0.01),且6周组高于4周组(P<0.05,P<0.01);哮喘4周和6周组支气管壁厚度、支气管平滑肌厚度及平滑肌细胞核数量均较对照组明显增加(P<0.01),且6周组高于4周组(P<0.01);哮喘4周和6周组的气道反应性均高于对照组(P<0.01),且6周组高于4周组(P<0.05)。结论PI3K信号通路可能通过促进气道平滑肌细胞增殖参与哮喘气道高反应性及气道重构过程。     

维生素D_3对缺乏维生素D的多囊卵巢综合征患者晚期糖基化终末产物受体的影响

目的研究维生素D3摄入对缺乏维生素D的多囊卵巢综合征(PCOS)患者血清AMH和sRAGE的影响。方法 54例患者分为25例缺乏维生素D合并PCOS的观察组和29例仅缺乏维生素D的对照组,给予口服8周维生素D3,检测口服前和口服8周后血清25-羟基维生素D(25 OH-D),AMH和sRAGE浓度。结果观察组和对照组摄入维生素D3后血清25 OH-D升高,且观察组血清sRAGE水平上升,AMH水平下降。结论缺乏维生素D合并PCOS患者摄入维生素D3可以通过增加sRAGE抑制AGEs的活性起到保护性作用。此外,维生素D3促进观察组患者血清AMH水平降低,改善卵泡生长发育环境。     

DNM3OS Facilitates Ovarian Cancer Progression by Regulating miR-193a-3p/MAP3K3 Axis

PurposeLong non-coding RNAs (lncRNAs) are essential regulators in the development of ovarian cancer (OC). Nonetheless, the function of lncRNA DNM3 opposite strand/antisense RNA (DNM3OS) in OC remains unclear. This work aimed to investigate the biological roles and underlying mechanisms of DNM3OS in OC.Materials and MethodsQuantitative real-time polymerase chain reaction was conducted to examine DNM3OS, microRNA (miR)-193a-3p, and mitogen-activated protein kinase 3 (MAP3K3) mRNA expression in OC tissues and cell lines. Kaplan-Meier survival analysis was employed to analyze the relationship between DNM3OS expression and the prognosis of OC patients. Cell counting kit-8, 5-ethynyl-2′-deoxyuridine, and transwell experiments were conducted to monitor cell proliferation, migration, and invasion, respectively. Western blot was applied to examine epithelial-mesenchymal transition associated protein (E-cadherin and N-cadherin) expression. Luciferase reporter gene and RNA immunoprecipitation experiments were performed to confirm the relationships among DNM3OS, miR-193a-3p, and MAP3K3. Pearson''s correlation analysis was adopted to analyze the correlations among DNM3OS, miR-193a-3p, and MAP3K3 mRNA.ResultsDNM3OS expression was remarkably increased in OC tissues and cell lines, which was associated with the unfavorable prognosis of the patients. DNM3OS overexpression enhanced OC cell proliferation, migration, and invasion; suppressed E-cadherin protein expression; and facilitated N-cadherin protein expression, while the transfection of miR-193a-3p mimics had the opposite effects. DNM3OS directly interacted with miR-193a-3p, and miR-193a-3p targeted MAP3K3 by directly binding to 3′UTR. DNM3OS could up-regulate the expression of MAP3K3 via repressing miR-193a-3p expression.ConclusionDNM3OS, as an oncogenic lncRNA, increases the malignancy of OC cells via regulation of an miR-193a-3p/MAP3K3 axis.     

STAT3和SOCS3与子宫内膜异位症的相关性研究

目的: 探讨信号转导和转录活化因子3(STAT3)和细胞因子信号转导抑制因子3(SOCS3)的表达与子宫内膜异位症的相关性。方法: 采用Western blotting方法检测30例子宫内膜异位症患者异位(异位组)、在位子宫内膜(在位组)和25例正常子宫内膜(对照组)中总STAT3、磷酸化STAT3(p-STAT3)和SOCS3蛋白的表达情况。结果: 总STAT3蛋白在3组内膜中表达无差异,而其活化水平(p-STAT3/STAT3)在异位组最高,SOCS3蛋白表达在异位组最低,两者与在位和对照组相比较差异有统计学意义(P<0.05),相关性分析显示内异症患者中STAT3活化水平与SOCS3蛋白表达呈负相关(r=-0.499, P<0.01)。结论: 在子宫内膜异位症患者的异位子宫内膜组织中存在STAT3过度活化和SOCS3蛋白表达下降,两者呈负相关。     

Assessment of chemical carcinogen-induced transforming activity using BALB/c-3T3 cells

Summary The BALB/c-3T3 cell transformation assay evaluates the morphologic transforming potential of test chemicals using cultured mammalian cells as targets. The assay is semiquantitative and employs a contact-inhibited clone of cells derived from the original BALB/c-3T3 mouse cell line. Transforming activity, or a focus, is recognized as a dense layer of morphologically altered cells superimposed on a monolayer of the normal cell phenotype. The induction of transforming activity in a standard assay has been reported to correlate well with the carcinogenicity of many test chemicals in rodent bioassay; however, the standard assay does not detect carcinogens of all chemical classes. This report describes an operational protocol for the standard BALB/c-3T3 cell transformation assay. In addition, it provides assay acceptance criteria and a discussion of a method to evaluate transforming activity data.     

Oocytes from Xenopus laevis contain an intrinsic σ2-like binding site

In preparation for expression studies for rat brain σ-binding sites, Xenopus oocytes were tested for the presence of [³H]di-o-tolylguanidine (DTG)-binding sites. Native oocytes were found to contain two intrinsic [³H]DTG-binding sites, a high-affinity site (K_d = 32 ± 6 nM, B_max of 45.7 ± 19 pmol/mg protein) and a low-affinity binding site (K_d = 1.3 ± 0.7 μM, B_max of 3.2 ± 0.7 nmol/mg protein). In a series of radioligand-binding-displacement studies, the high-affinity binding sites were found to have a binding profile which has a similar K_d to that of the mammalian σ₂-binding site (32 vs. 38 nM). Comparison of the IC₅₀ values for inhibition of [³H]DTG binding in rat liver and oocytes for DTG, haloperidol (HAL), (−)-pentazocine, (+)-3-(3-hydroxyphenyl)-N-propylpiperidine hydrochloride ((+)-3-PPP), (+(-pentazocine and Zn²⁺, showed similarity in rank (r² = 0.913) but a 7-fold lower potency in oocytes. These results suggest that the high-affinity [³H]DTG-binding site in oocytes represents a σ₂-like binding site.     

真核表达载体pLNCX/anti-CD20scFv/IgGFc/CD80/CD28/ζ的构建及其在NIH 3T3细胞株中的表达

目的: 构建pLNCX/anti-CD20scFv/IgGFc/CD80/CD28/ζ的重组真核表达载体，并在NIH 3T3细胞株中表达。方法: 采用DNA重组技术把pBULLET上的CD28-ζcDNA插入到已含anti-CD20 scFv/IgGFc/CD80的真核表达载体pLNCX质粒上，转染NIH 3T3细胞株，经G418筛选细胞，用RT-PCR、流式细胞术检测目的基因表达情况。结果: 经菌落PCR、酶切及一次测序鉴定均证实pLNCX/anti-CD20scFv/IgGFc/CD80/CD28/ζ的成功构建；经RT-PCR法，能够从转染的NIH 3T3细胞中扩增出1条与目的基因大小一致的DNA片段，流式细胞术检测显示该目的基因能够在NIH 3T3细胞中表达目的蛋白。结论: 重组表达载体pLNCX/anti-CD20scFv/IgGFc/CD80/CD28/ζ的构建，并在NIH 3T3细胞株中的成功表达，为该重组质粒转染原代T淋巴细胞从而制备CD20靶向性嵌合锚定T细胞奠定了基础。     

Covalent binding of guanine nucleotides to the CD3-γ chain of the T cell receptor/CD3 complex

In a search for proteins involved in signal transduction through the T cell receptor (TcR/CD3 complex), a recently developed highly efficient method for labeling of nucleotide binding proteins in permeabilized cells was applied. Here, we report that human CD3-γ could be labeled by periodate-oxidized [α-³²P] GTP (GTP_oxi). In contrast to GTP_oxi labeling of CD3-ξ, (Peter, M. E., Hall, C, Ruhlmann, A., Sancho, J. and Terhorst, C, EMBOJ. 1992. 11: 933), GTP-specific labeling of CD3-γ reached a maximum when nucleotides were added 60 min prior to the cross-linking reaction. As CD3-γ did not contain a known consensus sequence for nucleotide binding and since labeling kinetics of CD3-γ coincided with those of cytosolic GTP-binding proteins, labeling may have been caused by a GTP-binding protein. This putative protein was not T cell specific because labeling of CD3-γ could also be achieved when expressed in the endoplasmic reticulum of Chinese hamster ovary (CHO) cells. In CHO cells, labeling by GTP_oxi took place only when CD3-γ was associated with CD3-ξ, whereas labeling could not be established upon association of CD3-γ with CD3-δ or TcR α. The observation that CD3-γ was labeled without leaving the endoplasmic reticulum led to the hypothesis that the association of CD3-γ with a GTP-binding protein might be involved in an early step of the TcR/CD3 complex formation or transport.     

Partial 3q trisomy due to an unbalanced 3/10 translocation

A newborn with partial 3q trisomy is reported. This female, small for gestational age, had multiple dysmorphic features, including turricephaly, microcephaly, broad and flat nasal bridge, anteverted nares, small ears, short limbs, bilateral transverse palmar creases, and fifth finger clinodactyly. The patient expired at 20 hours of age. An autopsy demonstrated duplication of the vagina and cervix, a bicornuate uterus, and streak ovaries. Cytogenetic studies revealed the patient to be trisomic for the portion of 3q distal to band 21 [46,XX,-10,t(3;10) (q21;p15)]. The father was found to carry a balanced 3/10 translocation [46,XY,t(3;10) (q21;p15)].     

人类bcl—2cDNA在NIH／3T3细胞中的表达

将０．９１ｋｂ的含有完整开放阅读框的人类ｂｃｌ－２ｃＤＮＡ以正向克隆于逆不病毒载体ｐＬ－ＸＳＮ的ＥｃｏＲ１位点，经ＰＡ３１７细胞包装后感染ＮＩＨ／３Ｔ３细胞，筛选出Ｇ４１８抗性克隆，经免疫印迹证实人类ｂｃｌ－２ｃＤＮＡ在ＮＩＨ／３Ｔ３细胞中获得了表达，这一表达人类Ｂｃｌ－２蛋白的哺乳类细胞模型的建立探讨ｂｃｌ－２的作用机制及其与其它基因间关系的研究奠定了基础。