Disease Info Card

Protein Truncation Abnormality

Information about Protein Truncation Abnormality: characteristics, related genes and pathways, plus antibodies you can use for research. This page is being enriched constantly, if you see some information you would like this page to include please send your suggestions to us.

Overview of Protein Truncation Abnormality

Most recent studies have shown that Protein Truncation Abnormality shares some biological mechanisms with adenoma, adenomatous-polyposis-coli, ataxia-telangiectasia, carcinoma, colorectal-cancer, colorectal-neoplasms, dystrophy, germline-mutation-abnormality, malignant-neoplasm-of-breast, malignant-neoplasm-of-ovary, malignant-neoplasms, mammary-neoplasms, muscular-dystrophy, mutation-out-of-frame, neoplasms, neurofibromatoses, neurofibromatosis-1, ovarian-neoplasm, polyposis, polyps.

Among the many pathways, these few ones have gauged particular interests from scientists studying Protein Truncation Abnormality, and have been seen in publications frequently: Cell Adhesion, Cell Cycle, Cell Death, Cell Proliferation, Dna Repair, Embryo Development, Hypersensitivity, Localization, Methylation, Mismatch Repair, Mrna Splicing, Oncogenesis, Pathogenesis, Reflex, Reverse Transcription, Rna Splicing, Secretion, Spermatogenesis, Translation, Transport

Quite a number of genes have been found to play important roles in Protein Truncation Abnormality, such as APC, ATM, BEST1, BRCA1, BRCA2, CEL, DMD, FAP, GLMN, MLH1, MSH2, NF1, PLEC, PROC, PTCH1, STK11, TP53, TSC1. See what Boster has to offer for the research of these genes by clicking the gene name links below and view a more detailed info card/product listing for that gene.

In a later update, we will include information such as current drugs and therapy solutions as well as on-going and past clinical trials for this disease. Plesae stay updated.