Product Name: Alk (1089-1095) pY1092
Product Number: PE-04AGV95
Size: 200 µg      Price:47.00
1 mg      $US94.00
5 mg      206.00
Peptide Name: Alk (1089-1095) pY1092

Product Use: Services as a blocking peptide for use with the ALK-pY1092 rabbit polyclonal antibody (Cat. No.: AB-PK518) that is also available from Kinexus. This phosphopeptide may also be useful as a substrate for screening the phosphatase activity of protein phosphatases. The peptide sequence is located in the region between the Transmembrane and kinase catalytic domains. One of the major in vivo sites of phosphorylation in ALK. The effect of its phosphorylation is unclear.

Peptide Production Method: Solid-phase peptide synthesis

Peptide Origin: Homo sapiens

Peptide Sequence: MTD-pY-NPN

Peptide Modifications N Terminus: Free amino

Peptide Modifications C Terminus: βAla-Cys
Peptide Modifications Other: Phosphorylated

Peptide Molecular Mass Calculated: 1108.07 Da

Peptide Purity Percent after Synthesis and Purification: >95

Peptide Appearance: White powder

Peptide Form: Solid

Storage Conditions: -20°C

Related Product 1: Alk - pY1092 phosphosite-specific antibody (Cat. No.: AB-PK518)

Scientific Background: Alk is a protein-tyrosine kinase of the TK group and Alk family. It is a neuronal receptor for the ligands pleiotrophin (PTN), a secreted growth factor, and midkine (MDK), a PTN-related factor. Alk signals via MyD88 and is important in neuronal differentiation and development. Cancer-related mutations in human tumours point to a gain of function of the protein kinase. The active form of the protein kinase normally acts to promote tumour cell proliferation. Chromosomal rearrangments (most common), mutations, and amplifications with the Alk gene are associated with numerous tumours including: anaplastic large cell lymphomas, neuroblastomas, and non-small cell lung cancer. These fusion proteins, as well as other mutations and amplifications, likely confer heightened (possibly consititutive) phosphotransferase activity and promote cell growth and anti-apoptotic pathways such as the Akt and MAPK pathways. In Neuroblastoma 3 (NBLST3), there was constitutive activation, and Endoplasmic Reticulum or Golgi Apparatus localization when Alk had gain of function mutations with F1174I or F1174V (located in the kinase catalytic subdomain III) or R1275Q (located just before the kinase catalytic Subdomain VII). Translocations of the Alk gene resulting in fusion proteins with NPM1 are observed in 5-10% of non-Hodgkin lymphomas, with CARS and SEC31A in inflammatory myofibroblastic tumours (IMTs) and ALO17 in anaplastic large-cell lymphoma (ALCL). The genes C/EBPB, and BCL2A1 are essential for ALCL growth and transcriptionally induced by Alk.