PDGFRB & STAT5A Protein Protein Interaction Antibody Pair
- Known as:
- PDGFRB & STAT5A Protein Protein Interaction Antibody Pair
- Catalog number:
- DI0466
- Product Quantity:
- 1 Set
- Category:
- -
- Supplier:
- Abno
- Gene target:
- PDGFRB & STAT5A Protein Interaction Antibody Pair
Ask about this productRelated genes to: PDGFRB & STAT5A Protein Protein Interaction Antibody Pair
- Gene:
- PDGFRB NIH gene
- Name:
- platelet derived growth factor receptor beta
- Previous symbol:
- PDGFR
- Synonyms:
- JTK12, CD140b, PDGFR1
- Chromosome:
- 5q32
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-10-05
- Gene:
- STAT5A NIH gene
- Name:
- signal transducer and activator of transcription 5A
- Previous symbol:
- STAT5
- Synonyms:
- MGF
- Chromosome:
- 17q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-09
- Date modifiied:
- 2016-10-05
Related products to: PDGFRB & STAT5A Protein Protein Interaction Antibody Pair
Related articles to: PDGFRB & STAT5A Protein Protein Interaction Antibody Pair
- Androgenetic alopecia (AGA) is a common progressive scalp hair loss disorder that leads to baldness. This study aimed to identify core genes and pathways involved in premature AGA through an approach. - Source: PubMed
Publication date: 2023/06/09
Premanand AdaikalasamyReena Rajkumari Baskaran - Anaplastic large cell lymphoma (ALCL) is an aggressive non-Hodgkin T cell lymphoma commonly driven by NPM-ALK. AP-1 transcription factors, cJUN and JUNb, act as downstream effectors of NPM-ALK and transcriptionally regulate PDGFRβ. Blocking PDGFRβ kinase activity with imatinib effectively reduces tumor burden and prolongs survival, although the downstream molecular mechanisms remain elusive. - Source: PubMed
Publication date: 2022/08/31
Garces de Los Fayos Alonso IZujo LWiest IKodajova PTimelthaler GEdtmayer SZrimšek MKollmann SGiordano CKothmayer MNeubauer H ADey SSchlederer MSchmalzbauer B SLimberger TProbst CPusch OHögler STangermann SMerkel OSchiefer A IKornauth CPrutsch NZimmerman MAbraham BAnagnostopoulos JQuintanilla-Martinez LMathas SWolf PStoiber DStaber P BEgger GKlapper WWoessmann WLook T AGunning PTurner S DMoriggl RLagger SKenner L - Expression of the constitutively activated TEL/PDGFbetaR fusion protein is associated with the t(5;12)(q33;p13) chromosomal translocation found in a subset of patients with chronic myelomonocytic leukemia. TEL/PDGFbetaR activates multiple signal transduction pathways in cell-culture systems, and expression of the TEL-PDGFRB fusion gene induces myeloproliferative disease (MPD) in mice. We used gene-targeted mice to characterize the contribution of signal transducer and activator of transcription (Stat) and Src family genes to TEL-PDGFRB-mediated transformation in methylcellulose colony and murine bone marrow transduction/transplantation assays. Fetal liver hematopoietic stem and progenitor cells harboring targeted deletion of both Stat5a and Stat5b (Stat5ab(null/null)) genes were refractory to transformation by TEL-PDGFRB in methylcellulose colony assays. Notably, these cell populations were maintained in Stat5ab(null/null) fetal livers and succumbed to transformation by c-Myc. Surprisingly, targeted disruption of either Stat5a or Stat5b alone also impaired TEL-PDGFRB-mediated transformation. Survival of TPiGFP-->Stat5a(-/-) and TPiGFP-->Stat5a(+/-) mice was significantly prolonged, demonstrating significant sensitivity of TEL-PDGFRB-induced MPD to the dosage of Stat5a. TEL-PDGFRB-mediated MPD was incompletely penetrant in TPiGFP-->Stat5b(-/-) mice. In contrast, Src family kinases Lyn, Hck, and Fgr and the Stat family member Stat1 were dispensable for TEL-PDGFRB disease. Together, these data demonstrate that Stat5a and Stat5b are dose-limiting mediators of TEL-PDGFRB-induced myeloproliferation. - Source: PubMed
Publication date: 2007/01/11
Cain Jennifer AXiang ZhifuO'Neal JulieKreisel FriederikeColson AnnaLynnLuo HuiHennighausen LotharTomasson Michael H