|Positive WB detected in||HepG2 cells, Raji cells|
|Positive IHC detected in||human cervical cancer tissue|
Note: suggested antigen retrieval with TE buffer pH 9.0; (*) Alternatively, antigen retrieval may be performed with citrate buffer pH 6.0
|Western Blot (WB)||WB : 1:2000-1:10000|
|Immunohistochemistry (IHC)||IHC : 1:50-1:500|
|Sample-dependent, check data in validation data gallery|
14419-1-AP targets TCF12/HEB in WB, IHC, IF, ELISA applications and shows reactivity with human, mouse, rat samples.
|Tested Reactivity||human, mouse, rat|
|Cited Reactivity||human, mouse|
|Host / Isotype||Rabbit / IgG|
|Immunogen||TCF12/HEB fusion protein Ag5765|
|Full Name||transcription factor 12|
|Calculated molecular weight||73 kDa|
|Observed molecular weight||73 kDa|
|GenBank accession number||BC050556|
|Gene ID (NCBI)||6938|
|Purification Method||Antigen affinity purification|
|Storage Buffer||PBS with 0.02% sodium azide and 50% glycerol pH 7.3.|
|Storage Conditions||Store at -20°C. Stable for one year after shipment. Aliquoting is unnecessary for -20oC storage. 20ul sizes contain 0.1% BSA.|
The product of TCF12 gene (TCF12, also called HTF4 or HEB) is a member of helix-loop-helix (HLH) protein family [PMID:22130667]. TCF12 is a transcriptional regulator that involved in the initiation of neuronal differentiation. It 's also known as E proteins, and activates transcription by binding to the E box (5'-CANNTG-3'), because of their direct DNA (E-box) binding ability [PMID: 19204326]. TCF12 was shown to suppress E-cadherin expression during the early stages of renal tubular epithelial cell dedifferentiation [PMID:17202424].
TCF12 is mutated in anaplastic oligodendroglioma.
A non-canonical role for the proneural gene Neurog1 as a negative regulator of neocortical neurogenesis.
Tcf12, a Member of Basic Helix-loop-helix Transcription Factors, Mediates Bone Marrow Mesenchymal Stem Cell Osteogenic Differentiation in vitro and in vivo.
Inhibitor of Differentiation 4 (ID4) represses mammary myoepithelial differentiation via inhibition of HEB.
Tumor-specific usage of alternative transcription start sites in colorectal cancer identified by genome-wide exon array analysis.
Extensive gene-specific translational reprogramming in a model of B cell differentiation and Abl-dependent transformation.