There is still only 1 review devoted in full by Klenova et. al. to the entire CTCF & BORIS family of paralogous 11 ZF TransFactors evolved via duplication of an ancestral CTCF 11 ZFs conserved from Insects to Humans

CTCF has been discovered by Victor Lobanenkov in late 80's and subsequently cloned by Elena Klenova, Galina Filippova, Elena Pugacheva, Dmitry Loukinov in collaboration with other members of the so-named Victor's "CTCF & BORIS Discovery Teams" who are respectively responsible for both identification and characterization of the very first full-length CTCF cDNA clones isolated initially from birds (E. Klenova et. al. Mol. Cell. Biol., 1993) and secondly obtained together with mapping & sequencing an entire genomic CTCF loci from mice, rats, and humans (G. Filippova et. al. Mol. Cell. Biol., 1996) which included a stunning observation made with regard to a truly exceptional evolutionary preservation of individual amino acids across the whole CTCF DNA-Binding Domain ("CTCF DBD") comprised of 10 C2H2-class and 1 C2HC-ype Zinc Fingers (a.k.a. the central "11 ZF" CTCF DBD) since it was found to be almost 100% conserved throughout vertebrae evolution from CTCF in a bony fish (cloned from Zebra Fish by E. Pugacheva et. al. Gene, 2005) to CTCF in primates and CTCF in humans. Remarkably, when the same Lobanenkov' team have also cloned CTCF gene and CTCF cDNA from one of the most commonly used species of Insect' Kingdom (submitted by G.F. and V.L. into international "GenBank' repository by the year of 2000) and had published Drosophila CTCF (a.k.a. "dCTCF" by Hanlim Moon et. al. in 2005 EMBO Reports), it become clear that a truly ubiquitous 11 ZF CTCF proteins possess highly versatile functions in all multi-cellular organisms from Drososophila to humans. In addition to transcriptional silencing or activating in a context-dependent fashion, it organizes epigenetically controlled chromatin insulators that regulate imprinted genes in soma. Recently, we have identified a CTCF paralogue, termed BORIS for Brother of the Regulator of Imprinted Sites, that is expressed only in the testis. BORIS has the same exons encoding the 11 ZF domain as mammalian CTCF genes, and hence interacts with similar cis elements, but encodes amino and carboxy termini distinct from those in CTCF. Normally, CTCF and BORIS are expressed in a mutually exclusive pattern that correlates with re-setting of methylation marks during male germ cell differentiation. The antagonistic features of these two gene siblings are underscored by showing that while CTCF overexpression blocks cell proliferation, expression of BORIS in normally BORIS-negative cells promotes cell growth which can lead to transformation. The suggestion that BORIS directs epigenetic reprogramming at CTCF target sites impinges on the observations that human BORIS is not only abnormally activated in a wide range of human cancers, but also maps to the cancer-associated amplification region at 20q13. The sibling rivalry occasioned by aberrant expression of BORIS in cancer may interfere with normal functions of CTCF including growth suppression, and contribute to epigenetic dysregulation which is a common feature in human cancer.CCCTC结合因子（CTCF）由Victor Lobanenkov于20世纪80年代末发现，随后由Elena Klenova、Galina Filippova、Elena Pugacheva、Dmitry Loukinov与以Victor命名的“CTCF与BORIS研究团队”的其他成员共同完成克隆。该团队先后开展了两项关键性工作：其一，首次从鸟类中分离得到全长CTCF cDNA克隆（E. Klenova等，《Molecular and Cellular Biology》，1993年）并对其进行鉴定与表征；其二，联合完成了小鼠、大鼠及人类全基因组CTCF基因座的定位与测序（G. Filippova等，《Molecular and Cellular Biology》，1996年）。其中一项令人瞩目的观测结果显示：由10个C2H2型锌指（C2H2-class Zinc Finger）与1个C2HC型锌指（C2HC-type Zinc Finger）组成的完整CTCF DNA结合结构域（CTCF DNA-binding domain，简称CTCF DBD，又称中央“11锌指（11 ZF）”CTCF DBD），其单个氨基酸残基在进化中具有极高的保守性。该结构域在从硬骨鱼（E. Pugacheva等2005年于《Gene》期刊报道，从斑马鱼中克隆得到CTCF）到灵长类再到人类的脊椎动物进化历程中，保守性近乎100%。值得注意的是，Lobanenkov团队还从昆虫纲最常用的模式物种之一中克隆了CTCF基因及cDNA（该序列由G.F.与V.L.于2000年提交至国际GenBank数据库），且Hanlim Moon等人于2005年在《EMBO Reports》发表了果蝇CTCF（又称“dCTCF”）的相关研究，由此证实，这种广泛存在的11锌指CTCF蛋白在从果蝇到人类的所有多细胞生物中均发挥着高度多样的生物学功能。除了以情境依赖的方式调控转录沉默或激活之外，CTCF还可组织表观遗传调控的染色质绝缘子，进而调节体细胞中的印记基因表达。近期，研究团队鉴定出了CTCF的旁系同源基因——印记位点调节因子兄弟（Brother of the Regulator of Imprinted Sites，简称BORIS），该基因仅在睾丸组织中表达。BORIS编码11锌指结构域的外显子序列与哺乳动物CTCF基因完全一致，因此可与相似的顺式作用元件结合，但其编码的氨基端与羧基端序列与CTCF存在显著差异。正常情况下，CTCF与BORIS的表达模式相互排斥，这与雄性生殖细胞分化过程中甲基化标记的重置过程密切相关。这两个基因同源物的拮抗特性可通过以下实验得到证实：过表达CTCF会抑制细胞增殖，而在原本不表达BORIS的细胞中异位表达BORIS则会促进细胞生长，甚至可引发细胞转化。有研究指出，BORIS可在CTCF靶位点介导表观遗传重编程，这与此前的观测结果相契合——人类BORIS不仅在多种人类癌症中异常激活，其编码基因还定位于20q13这一与癌症相关的扩增区域。BORIS在癌症中异常表达所引发的同源基因竞争，可能会干扰CTCF的正常功能（包括生长抑制作用），进而促成表观遗传失调，而这正是人类癌症的常见特征之一。