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受体“Ck”缺陷会引发白血病吗?

Does receptor-'Ck' deficiency initiate leukaemia?

作者信息

Kaul D, Singh J

机构信息

Department of Experimental Medicine and Biotechnology, Postgraduate Institute of Medical Education and Research, Chandigarh, India.

出版信息

Cancer Lett. 1997 Jan 30;112(2):199-202. doi: 10.1016/s0304-3835(96)04570-3.

DOI:10.1016/s0304-3835(96)04570-3
PMID:9066728
Abstract

We have developed a polyclonal monospecific antibody (designated Ab-Ck) which recognises specifically a novel cell surface Receptor-'Ck', having inherent ability to regulate mevalonate pathway that is vital for many cellular functions ranging from growth control to differentiation. By using this 'Ab-Ck' as a probe, the Western blot analysis of protein fractions derived from various types of normal and cancerous cells/tissues revealed not only that this Receptor-'Ck' was ubiquitously present in various human organs, especially adrenal cortex, aorta, liver and brain, but also that leukaemic cell lines as well as lymphocytes from CML patients were specifically and selectively deficient in this receptor. Based upon these observations, we propose that leukaemic process may be initiated as a consequence of the deficiency of this novel Receptor-'Ck'.

摘要

我们已经研发出一种多克隆单特异性抗体(命名为Ab-Ck),它能特异性识别一种新型细胞表面受体——“Ck”,该受体具有调节甲羟戊酸途径的内在能力,而甲羟戊酸途径对从生长控制到分化等许多细胞功能至关重要。通过使用这种“Ab-Ck”作为探针,对来自各种正常和癌细胞/组织的蛋白质组分进行蛋白质免疫印迹分析发现,不仅这种受体——“Ck”普遍存在于各种人体器官中,尤其是肾上腺皮质、主动脉、肝脏和大脑,而且白血病细胞系以及慢性粒细胞白血病患者的淋巴细胞中该受体存在特异性和选择性缺陷。基于这些观察结果,我们提出白血病过程可能是由于这种新型受体——“Ck”的缺陷而引发的。

相似文献

1
Does receptor-'Ck' deficiency initiate leukaemia?受体“Ck”缺陷会引发白血病吗?
Cancer Lett. 1997 Jan 30;112(2):199-202. doi: 10.1016/s0304-3835(96)04570-3.
2
LDL-dependent regulation of Bcl-2 and cyclin 'D' gene expression in lymphocytes from normal and CML patients.正常人和慢性粒细胞白血病患者淋巴细胞中低密度脂蛋白(LDL)对Bcl-2和细胞周期蛋白D基因表达的调控
Cancer Lett. 1997 Nov 11;119(2):131-5. doi: 10.1016/s0304-3835(97)00266-8.
3
Receptor-'Ck' dependent signalling regulates the LDL-receptor gene transcription.受体“Ck”依赖性信号传导调节低密度脂蛋白受体基因转录。
Mol Cell Biochem. 1997 Apr;169(1-2):79-83. doi: 10.1023/a:1006806118493.
4
RNA-mediated regulation of Receptor-Ck gene in human platelets.
Mol Cell Biochem. 1997 Aug;173(1-2):189-92. doi: 10.1023/a:1006872904778.
5
Potential role of Notch signalling in CD34+ chronic myeloid leukaemia cells: cross-talk between Notch and BCR-ABL.Notch信号通路在CD34+慢性髓性白血病细胞中的潜在作用:Notch与BCR-ABL之间的相互作用
PLoS One. 2015 Apr 7;10(4):e0123016. doi: 10.1371/journal.pone.0123016. eCollection 2015.
6
Expression of bcr-abl mRNA in individual chronic myelogenous leukaemia cells as determined by in situ amplification.
Br J Haematol. 2001 Mar;112(3):749-59. doi: 10.1111/j.1365-2141.2001.02510.x.
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Chronic myelogenous leukaemia exosomes modulate bone marrow microenvironment through activation of epidermal growth factor receptor.慢性粒细胞白血病外泌体通过激活表皮生长因子受体调节骨髓微环境。
J Cell Mol Med. 2016 Oct;20(10):1829-39. doi: 10.1111/jcmm.12873. Epub 2016 May 14.
8
The P190, P210, and P230 forms of the BCR/ABL oncogene induce a similar chronic myeloid leukemia-like syndrome in mice but have different lymphoid leukemogenic activity.BCR/ABL癌基因的P190、P210和P230形式在小鼠中诱导出类似慢性髓性白血病的综合征,但具有不同的淋巴细胞白血病致瘤活性。
J Exp Med. 1999 May 3;189(9):1399-412. doi: 10.1084/jem.189.9.1399.
9
[Overexpression of Shp-2 is associated with the unlimited growth and apoptosis resistance of p210 bcr-abl-mediated chronic myeloid leukemia].[Shp-2的过表达与p210 bcr-abl介导的慢性髓性白血病的无限增殖和凋亡抵抗相关]
Zhonghua Yi Xue Za Zhi. 2005 Jul 20;85(27):1903-6.
10
The Potential of Exosomes Derived from Chronic Myelogenous Leukaemia Cells as a Biomarker.源自慢性粒细胞白血病细胞的外泌体作为生物标志物的潜力
Anticancer Res. 2018 Jul;38(7):3935-3942. doi: 10.21873/anticanres.12679.

引用本文的文献

1
Receptor Ck-dependent signaling regulates hTERT gene transcription.受体Ck依赖性信号传导调节hTERT基因转录。
BMC Cell Biol. 2006 Jan 12;7:2. doi: 10.1186/1471-2121-7-2.
2
Receptor-Ck regulates the expression of cyclin-dependent kinase inhibitors (p16; p27).
Mol Cell Biochem. 1999 Oct;200(1-2):183-6. doi: 10.1023/a:1006981614054.