LKB1 Blocking Peptide
- Known as:
- LKB1 Blocking Peptide
- Catalog number:
- 33r-11022
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- LKB1 Blocking Peptide
Related genes to: LKB1 Blocking Peptide
- Gene:
- STK11 NIH gene
- Name:
- serine/threonine kinase 11
- Previous symbol:
- -
- Synonyms:
- PJS, LKB1
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-01-21
- Date modifiied:
- 2019-04-23
- Gene:
- STK11IP NIH gene
- Name:
- serine/threonine kinase 11 interacting protein
- Previous symbol:
- -
- Synonyms:
- LIP1, KIAA1898, LKB1IP, STK11IP1
- Chromosome:
- 2q35
- Locus Type:
- gene with protein product
- Date approved:
- 2002-09-12
- Date modifiied:
- 2014-11-19
Related products to: LKB1 Blocking Peptide
Related articles to: LKB1 Blocking Peptide
- Lobular endocervical glandular hyperplasia (LEGH) is a benign cervical condition that has been proposed as a precursor lesion to minimal deviation adenocarcinoma (MDA), a rare but highly aggressive subtype of well-differentiated gastric-type endocervical adenocarcinoma (GAS). MDA is more frequently observed in patients with Peutz-Jeghers syndrome (PJS) and is strongly associated with mutations in the STK11 gene. While LEGH is not inherently linked to PJS, its potential progression to MDA warrants vigilance, particularly in patients with PJS due to their heightened risk of gynecologic malignancies. Here, we report a case of LEGH diagnosed during surveillance for PJS, analyzed via whole genome sequencing. LEGH is a benign cervical condition, considered a precursor lesion to minimal deviation adenocarcinoma, often observed in patients with Peutz-Jeghers syndrome (PJS) and potentially linked to mutations in the gene. - Source: PubMed
Publication date: 2025/01/16
Ichinose TakayukiTakasaki KazukiTakahashi YukoHirano ManaNishida HarukaHiraike HarukoSasajima YukoNagasaka Kazunori - Many recent efforts to analyze cancer genomes involve aggregation of mutations within reference maps of molecular pathways and protein networks. Here, we find these pathway studies are impeded by molecular interactions that are functionally irrelevant to cancer or the patient's tumor type, as these interactions diminish the contrast of driver pathways relative to individual frequently mutated genes. This problem can be addressed by creating stringent tumor-specific networks of biophysical protein interactions, identified by signatures of epistatic selection during tumor evolution. Using such an evolutionarily selected pathway (ESP) map, we analyze the major cancer genome atlases to derive a hierarchical classification of tumor subtypes linked to characteristic mutated pathways. These pathways are clinically prognostic and predictive, including the TP53-AXIN-ARHGEF17 combination in liver and CYLC2-STK11-STK11IP in lung cancer, which we validate in independent cohorts. This ESP framework substantially improves the definition of cancer pathways and subtypes from tumor genome data. - Source: PubMed
Publication date: 2018/10/08
Wang ShengMa JianzhuZhang WeiShen John PaulHuang JustinPeng JianIdeker Trey - Signal transduction by the Smad pathway elicits critical biological responses to many extracellular polypeptide factors, including TGFβ and bone morphogenetic protein. Regulation of Smad signaling imparts several cytoplasmic and nuclear mechanisms, some of which entail protein phosphorylation. Previous work established a protein complex between Smad4 and the scaffolding protein LKB1-interacting protein 1 (LIP1). LKB1 is a well studied tumor suppressor kinase that regulates cell growth and polarity. Here, we analyzed the LKB1-LIP1 and the Smad4-LIP1 protein complexes and found that LIP1 can self-oligomerize. We further demonstrate that LKB1 is capable of phosphorylating Smad4 on Thr(77) of its DNA-binding domain. LKB1 inhibits Smad4 from binding to either TGFβ- or bone morphogenetic protein-specific promoter sequences, which correlates with the negative regulatory effect LKB1 exerts on Smad4-dependent transcription. Accordingly, LKB1 negatively regulates TGFβ gene responses and epithelial-mesenchymal transition. Thus, LKB1 and LIP1 provide negative control of TGFβ signaling. - Source: PubMed
Publication date: 2010/10/25
Morén AnitaRaja ErnaHeldin Carl-HenrikMoustakas Aristidis - Peutz-Jeghers syndrome (PJS) is typically manifested as severe gastrointestinal polyposis. Polyps in PJS patients and in Lkb1(+/-) mice that model PJS polyposis are frequently characterized by elevated cyclooxygenase-2 (COX-2). This study was designed to determine whether COX-2 inhibition would reduce tumor burden in Lkb1(+/-) mice or Peutz-Jeghers patients. - Source: PubMed
Udd LinaKatajisto PekkaRossi Derrick JLepistö AnnaLahesmaa Anna-MariaYlikorkala AnttiJärvinen Heikki JRistimäki Ari PMäkelä Tomi P - Specialized cells that form barriers such as those of the intestine adopt a distinct asymmetry. One particular protein may be a prime mover in bringing about such cellular organization. - Source: PubMed
Nelson W James