panTRK, Rmab Antibody from MyBioSource.com

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panTRK, Rmab Antibody

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The panTRK, Rmab Antibody from MyBioSource.com is a Rabbit Monoclonal antibody. The panTRK, Rmab Antibody has been shown to work in the following applications: Immunohistochemistry, Immunohistochemistry - fixed, and Immunohistochemistry - frozen.

Description

TRK (tropomyosin receptor kinase) A, B, and C are encoded by NTRK1, NTRK2, and NTRK3 genes respectively. Each protein is activated by different neurotrophins: TRKA is activated by Nerve growth factor, TRKB by brain-derived neurotrophic factor, and TRKC by NT-3. The TRK receptors are a family of tyrosine kinases that regulate synaptic strength and plasticity in the mammalian nervous system. The activation of TRK receptors by neurotrophin binding may lead to activation of signal cascades resulting in promoting survival and other functional regulation of cells. TRK family of receptor tyrosine kinases are of interest as the NTRK genes that encode them are involved in gene fusions identified in a wide range of adult and pediatric tumors. TRK, was initially identified in a colon carcinoma, is frequently activated in thyroid papillary carcinomas.

Pan-TRK IHC has shown to be positive in most cases with NTRK fusion transcripts confirmed by Archer. One study established the Pan-TRK IHC sensitivity and specificity for transcribed NTRK fusions to be 95.2% and 100%, respectively. All positive IHC cases had cytoplasmic staining while the following fusion partner-specific patterns were discovered: all LMNA-NTRK1 fusions displayed nuclear membrane accentuation, all TPM3/4 fusions displayed cellular membrane accentuation, and half of ETV6-NTRK3 fusions displayed nuclear staining. In another study, Immunohistochemistry screening in 1043 various solid tumors showed TRKA expression in 1.6% of samples, including Colorectal, Lung Cancer, Biliary Carcinoma and Thyroid Cancers. NTRK gene fusions have been identified in both pediatric and adult primary central nervous system tumors, including Glioblastoma Multiforme, Pediatric Gliomas and Astrocytomas. Various translocations involving NTRK1 or NTRK3 have been reported in Spitzoid melanocytic neoplasms, as well as in compound Spitz Nevi. TRK fusions have also been reported in Intrahepatic Cholangiocarcinomas, Breast Cancer, quadruple wild-type (ETV6-NTRK3) Gastrointestinal Stromal Tumors, Gallbladder Adenocarcinomas, Pancreatic Carcinomas, Sinus-Nasal Low-Grade Non-Intestinal-type Adenocarcinomas and Neuroendocrine Tumors of the small bowel. In addition to being present in solid tumors, NTRK gene fusions have been also detected in Acute Lymphoblastic Leukemia and Acute Myeloid Leukemia