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Human Monoclonal TCL1A Primary Antibody for IHC (fro), IHC (p) - ABIN1109210
Rodig, Vergilio, Shahsafaei, Dorfman: Characteristic expression patterns of TCL1, CD38, and CD44 identify aggressive lymphomas harboring a MYC translocation. in The American journal of surgical pathology 2007
Show all 7 Pubmed References
Human Polyclonal TCL1A Primary Antibody for WB - ABIN1944776
Virgilio, Narducci, Isobe, Billips, Cooper, Croce, Russo: Identification of the TCL1 gene involved in T-cell malignancies. in Proceedings of the National Academy of Sciences of the United States of America 1995
Show all 4 Pubmed References
Human Polyclonal TCL1A Primary Antibody for ELISA, WB - ABIN547887
Shen, Ferguson, Renard, Hoyer, Kim, Hao, Alt, Roeder, Morse, Teitell: Dysregulated TCL1 requires the germinal center and genome instability for mature B-cell transformation. in Blood 2006
Human Polyclonal TCL1A Primary Antibody for WB - ABIN4890302
Ho, Bongartz, Liu, Kalari, Goss, Shepherd, Goetz, Kubo, Ingle, Wang, Weinshilboum: Estrogen, SNP-Dependent Chemokine Expression and Selective Estrogen Receptor Modulator Regulation. in Molecular endocrinology (Baltimore, Md.) 2016
acalabrutinib showed increased BTK selectivity compared with ibrutinib while demonstrating significant antitumor efficacy in vivo on par with ibrutinib. Similarly, in the TCL1 adoptive transfer model, decreased phosphorylation of BTK, PLCgamma2, and S6 was observed. Most notably, treatment with acalabrutinib resulted in a significant increase in survival compared with mice receiving vehicle
suggests that in the TCL1-tg mouse, main tumor support may not be derived from CD4+ T cells, but from the monocytic population
we revealed that one of the key functions of KLF4-induced TCL1 during reprogramming is to promote the metabolic shift from oxidative phosphorylation to glycolysis.
results indicate that decreased Cav-1 in Emu-TCL1 mice significantly delays the onset of CLL and decreases leukemic progression by inhibiting MAPK-Erk signaling, suggesting a role for Cav-1 in the proliferation and progression of CLL
This review discusses the main features of the original TCL1 models and the different lines of research successively developed with particular attention to genetically compound mice and the therapeutic applications in drug development.
Tcl1 expression downregulated a distinct group of genes, including Ndp52, whose expression is very high in blastocysts but reduced in the primitive ectoderm.
Data indicate that APRIL expression accelerates the onset of TCL1-driven leukemia formation mainly through TACI activation.
These findings demonstrate cooperation of Tcl1 and the NF-kB pathway in the pathogenesis of aggressive chronic lymphocytic leukemia.
An important role of TCL1 in activating the ER stress response in support for malignant progression of chronic lymphocytic leukemia.
TCL1 and/or other genes in the TCL1 pathway are responsible for the initiation of human chronic lymphocytic leukemia.
role in early embryonic development and overexpression in human seminomas
Akt kinase activity can be inhibited by a peptide spanning the betaA strand of the proto-oncogene TCL1
Tcl1 is a coactivator of Akt signaling, in normal T- and B-cell development and function.
Detailed mechanism for TCL1-augmented signaling helps explain the delayed occurrence of mature T cell expansions and leukemias despite tumorigenic TCL1 dysregulation that begins in early thymocytes.
findings indicate that other oncogenic mechanism(s) may be involved in the development of solid tumors in Emu-TCL1 transgenic mice
TCL1 transgenic B cells primed for transformation must experience the germinal center environment and, for at least some, develop genome instability to become fully malignant.
Data indicate that the immunoglobulin heavy and light chain rearrangements in TCL1 mice display minimal levels of somatic mutations and exhibit several molecular features found in the human disease.
early mouse embryos display a physiological dissociation between TCL1 functions of AKT phosphorylation and phosphorylated AKT transfer to nucleus
a ternary complex of TCL1, Epac1, and Akt forms in activated macrophages both promoting Akt activation and regulating intracellular distribution of Akt
Tcl1 gene(s) might have important roles in hair formation, by its involvement in cycling and self-renewal of transient amplifying (TA) and stem-cell (SC) populations.
Combination of T-cell lymphoma-1 protein (TCL1)-overexpression and damaging ataxia telangiectasia mutated protein (ATM) functionally synergistically contribute to T-cell prolymphocytic leukemia (T-PLL) specific phenotype of impaired DNA damage processing.
Case Report: hematogones can express TCL-1 in patients with T-cell prolymphocytic leukemia after therapy.
TCL1A is not only a useful biomarker for prognostic evaluation in stage II/III colorectal cancer patients.
Our results suggest that intratumoral TCL1A+ B cells are important for controlling cervical cancer development.
Our study suggests that TCL1 expression profile may have a role in the prediction of overall outcome in patient with MCL and call for prospective studies.
We investigated TCL1 expression at the protein level in the bone marrow of a series of 59 patients with Waldenstrom macroglobulinemia: 76% of patients expressed TCL1, which appeared to be associated with a pejorative prognostic impact.
Suggest miR-181b as therapeutic target for chronic lymphocytic leukemia in the Emicro-TCL1 mouse model.
High TCL1A expression is associated with chronic lymphocytic leukemia.
Polymorphic genetic variations of cytochrome P450 19A1 and T-cell leukemia 1A genes in the Tamil population
Peptide-based TCL1-interphase mimics were potent in steric AKT antagonization.
demonstrated that miR-3676 targets three consecutive 28-bp repeats within 3'UTR of TCL1 and showed that miR-3676 is a powerful inhibitor of TCL1
Case Report: T-cell lymphoblastic leukemia/lymphoma with t(7;14)(p15;q32) [TCRgamma-TCL1A translocation] confirmed by FISH.
Report frequent TCL1A rearrangements in T-cell prolymphocytic leukemia with cutaneous involvement.
TCL1-Tg:p53(-/-) leukemia cells exhibit higher survival capacity and are more drug resistant than the leukemia cells from TCL1-Tg:p53wt mice
TCL1A and ATM are co-expressed in chronic lymphocytic leukemia cells without deletion of 11q.
SNPs near the 3' terminus of TCL1A were associated with aromatase inhibitors-dependent musculoskeletal pain. Estradiol induced SNP-dependent TCL1A expression.
Data indicate that up-regulated transcription of TCL1A was observed in two cases.
Our findings reveal a functional interaction between Tcl1 and Hsp70 and identify Tcl1 as a novel Hsp70 client protein
Intracellular expression of the TCL1 as well as membrane and intracellular expression of ILT7 in plasmacytoid dendritic cell leukemia (pDCL) samples and 61 non-pDC acute leukemia samples, were tested.
These findings demonstrate that the microenvironment has a proactive role in the regulation of the known signaling enhancer and pro-survival molecule TCL1 in CLL.
Overexpression of the TCL1 gene in humans has been implicated in the development of mature T cell leukemia, in which chromosomal rearrangements bring the TCL1 gene in close proximity to the T-cell antigen receptor (TCR)-alpha (MIM 186880) or TCR-beta (MIM 186930) regulatory elements (summarized by Virgilio et al., 1998
T-cell leukemia/lymphoma 1A
, T-cell lymphoma-1
, T-cell leukemia/lymphoma protein 1A
, T-cell lymphoma breakpoint 1
, oncogene TCL-1
, oncogene TCL1
, protein p14 TCL1
, T-cell leukemia/lymphoma protein 1A (P14 TCL1 protein) (TCL1 oncogene) (TCL-1 protein)