Anti-TCL1B (aa 64-125) polyclonal antibody

The members of the TCL1 proto-oncogene family (TCL1, MTCP1, and TCL1b) bind to Akt1, increasing its phosphorylation status and kinase activity. This is thought to be secondary to the formation of TCL1-Akt oligomers within which Akt is preferentially phosphorylated. Here we show that, in contrast to Akt1 and Akt2, which bind to all members of the TCL1 family, Akt3 specifically interacts with TCL1 but not with MTCP1 or TCL1b. This association is functional, as the presence of TCL1 but not MTCP1 or TCL1b increased Akt3 kinase activity in in vitro kinase assays. Functional specificity is determined by the Akt pleckstrin homology domain as chimeric Akt1, where Akt1 PH domain was replaced by that of Akt3 was no longer able to interact with MTCP1 or TCL1b and its kinase activity was solely enhanced by TCL1 Moreover, we show that, in TCL1-overexpressing SUPT-11 T-cell leukemia and P3HR-1 Burkitt's lymphoma cell lines, TCL1 interacts with endogenous Akt1, Akt2, and Akt3. TCL1 enhanced hetero-oligomerization of Akt1 with Akt3 and as a consequence facilitated transphosphorylation of Akt molecules, which may contribute to Akt activation and TCL1-induced leukemogenesis in vivo.

Objective: We present prenatal diagnosis and molecular cytogenetic characterization of a de novo 3.19-Mb chromosome 14q32.13-q32.2 deletion of paternal origin. Case report: A 36-year-old woman underwent amniocentesis at 20 weeks of gestation because of an advanced maternal age. Her husband was 36 years old. Amniocentesis revealed a karyotype of 46,XY,del(14)(q32.1q32.2). Simultaneous array comparative genomic hybridization (aCGH) analysis showed the result of a 14q32.13-q32.2 deletion. Prenatal ultrasound was unremarkable. The parental karyotypes were normal and did not have such a deletion. The pregnancy was subsequently terminated, and a malformed fetus was delivered with facial dysmorphism. aCGH was applied on the DNA extracted from cord blood. Polymorphic DNA marker analysis was applied on the DNAs extracted from placenta and parental bloods. aCGH confirmed a 3.19-Mb 14q32.13-q32.2 deletion or arr 14q32.13q32.2 (96,151,751-99,341,476) x 1.0 [GRCh37 (hg19)] encompassing 10 Online Mendelian Inheritance in Man (OMIM) genes of TCL1B, TCL1A, TUNAR, BDKRB2, BDKRB1, ATG2B, GSKIP, AK7, PAPOLA and VRK1. Polymorphic DNA marker analysis confirmed a paternal origin of a de novo interstitial distal 14q deletion. Conclusion: Determination of the paternal origin of a prenatally detected de novo interstitial distal 14q deletion by polymorphic DNA marker analysis in this case is significant, and the information acquired is useful for genetic counseling, especially when amniocentesis is performed because of an advanced maternal age. (C) 2020 Taiwan Association of Obstetrics & Gynecology. Publishing services by Elsevier B.V.