生物来源
mouse
质量水平
抗体形式
purified antibody
抗体产品类型
primary antibodies
克隆
BTL73, monoclonal
纯化方式
affinity chromatography
种属反应性
human
制造商/商品名称
Upstate®
技术
immunohistochemistry: suitable
western blot: suitable
同位素/亚型
IgG1κ
NCBI登记号
UniProt登记号
运输
wet ice
基因信息
human ... TAL1(6886)
一般描述
TAL-1, also known as SCL (stem cell leukemia), is a serine phosphoprotein and basic-helix-loop-helix transcription factor. TAL-1 is implicated in the genesis of hemopoietic malignancies and is a positive regulator of erythroid differentiation. A nonrandom, site-specific TAL-1 chromosomal translocation is commonly associated with oncogenic transformation in many T-cell acute lymphoblastic leukemias. TAL-1 binds to the LIM domain containing protein Rhombotin 2 (RBTN2), where it forms a complex with GATA1 or GATA 2 that is essential for erythropoiesis.
特异性
This antibody detects two predominant protein products of the SCL/TAL1 gene in T cell acute lymphoblastic leukemia (T-ALL): a full length PP42-TAL1 (42/44 kDa) and a truncated form PP24-TAL1 (24/26 kDa).
免疫原
Epitope: C-Terminus
Recombinant GST-TAL1 (K Pulford, et al., 1995, Blood, 85: 675 - 684)
应用
Research Category
Epigenetics & Nuclear Function
Epigenetics & Nuclear Function
Research Sub Category
Transcription Factors
Transcription Factors
Use Anti-TAL-1 Antibody, clone BTL73 (Mouse Monoclonal Antibody) validated in WB, IHC to detect TAL-1 also known as SCL, T-cell acute lymphocytic leukemia 1, TCL5, TAL-1, Stem cell protein.
Western Blot Analysis: 2 μg/mL of this lot detected a strong 44 kDa of PP42-TAL1 in Jurkat cell lysate, and also very faint PP24-TAL. Optimal working dilutions must be determined by the end user.
质量
Routinely evaluated by western blot on Jurkat cell lysate.
目标描述
44 kDa
外形
Protein G Purified
Purified mouse monoclonal IgG1k in buffer containing PBS and 0.05% sodium azide.
储存及稳定性
Stable for 1 year at 2-8°C from date of receipt. Avoid repeated freeze/thaw cycles, which may damage IgG and affect product performance.
分析说明
Control
Jurkat cell lysate
Jurkat cell lysate
其他说明
Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.
法律信息
UPSTATE is a registered trademark of Merck KGaA, Darmstadt, Germany
免责声明
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
WGK
WGK 2
闪点(°F)
Not applicable
闪点(°C)
Not applicable
A 3-bp deletion in the HBS1L-MYB intergenic region on chromosome 6q23 is associated with HbF expression.
Farrell, JJ; Sherva, RM; Chen, ZY; Luo, HY; Chu, BF; Ha, SY; Li, CK; Lee, AC; Li, RC; Li et al.
Blood null
Suppression of super-enhancer-driven TAL1 expression by KLF4 in T-cell acute lymphoblastic leukemia.
Mina Noura et al.
Oncogene, 43(6), 447-456 (2023-12-16)
TAL1 is one of the most frequently dysregulated genes in T-ALL and is overexpressed in about 50% of T-ALL cases. One of the molecular mechanisms of TAL1 overexpression is abnormal mutations in the upstream region of the TAL1 promoter that
Riadh Lobbardi et al.
Cancer discovery, 7(11), 1336-1353 (2017-10-05)
T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive malignancy of thymocytes. Using a transgenic screen in zebrafish, thymocyte selection-associated high mobility group box protein (TOX) was uncovered as a collaborating oncogenic driver that accelerated T-ALL onset by expanding the initiating
Charlotte Smith et al.
Haematologica (2023-01-13)
T-cell acute lymphocytic leukemia protein 1 (TAL1) is one of the most frequently deregulated oncogenes in T-cell acute lymphoblastic leukemia (T-ALL). Its deregulation can occur through diverse in cis-alterations, including SIL-TAL1 microdeletions, translocations with Tcell Receptor (TCR) loci and, more
Mark A Gillespie et al.
Molecular cell, 78(5), 960-974 (2020-04-25)
Dynamic cellular processes such as differentiation are driven by changes in the abundances of transcription factors (TFs). However, despite years of studies, our knowledge about the protein copy number of TFs in the nucleus is limited. Here, by determining the
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