Validation Data Gallery
|Positive IHC detected in||human breast cancer tissue, human colon tissue, human colon cancer tissue, human endometrial cancer tissue|
Note: suggested antigen retrieval with TE buffer pH 9.0; (*) Alternatively, antigen retrieval may be performed with citrate buffer pH 6.0
|Immunohistochemistry (IHC)||IHC : 1:20-1:200|
|Sample-dependent, check data in validation data gallery|
19782-1-AP targets APC in WB, IHC applications and shows reactivity with human samples.
|Host / Isotype||Rabbit / IgG|
|Full Name||adenomatous polyposis coli|
|Calculated molecular weight||312 kDa|
|GenBank accession number||NM_000038|
|Gene ID (NCBI)||324|
|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.|
APC, also named as DP2.5, belongs to the adenomatous polyposis coli (APC) family. APC is a tumor suppressor that regulates cell division, helps ensure that the number of chromosomes in a cell is correct following cell division, and associates with other proteins involved in cell attachment and signaling. APC promotes rapid degradation of CTNNB1 and participates in Wnt signaling as a negative regulator. It plays a critical role in several cellular processes. APC regulates beta-catenin levels through Wnt-signaling and is involved in actin cytoskeletal integrity, cell-cell adhesion and cell migration. APC activity is correlated with its phosphorylation state. Defects in APC are a cause of familial adenomatous polyposis (FAP) which includes also Gardner syndrome (GS). Defects in APC are a cause of hereditary desmoid disease (HDD) which also known as familial infiltrative fibromatosis (FIF). Defects in APC are a cause of medulloblastoma (MDB) which is a malignant, invasive embryonal tumor of the cerebellum with a preferential manifestation in children. Defects in APC are a cause of mismatch repair cancer syndrome (MMRCS) which also known as Turcot syndrome or brain tumor-polyposis syndrome 1 (BTPS1).
J Bone Oncol
BAIAP2L2 promotes the proliferation, migration and invasion of osteosarcoma associated with the Wnt/β-catenin pathway
MiR-26b suppresses hepatocellular carcinoma development by negatively regulating ZNRD1 and Wnt/β-catenin signaling.
World J Gastroenterol
MiR-205 mediated APC regulation contributes to pancreatic cancer cell proliferation.
Glycogen phosphorylase B promotes ovarian cancer progression via Wnt/β-catenin signaling and is regulated by miR-133a-3p.
Norepinephrine-CREB1-miR-373 axis promotes progression of colon cancer.
The reviews below have been submitted by verified Proteintech customers who received an incentive forproviding their feedback.
Brianna (Verified Customer) (12-13-2018)