TPO _ THPO Antibody
- Known as:
- TPO _ THPO Antibody
- Catalog number:
- 10381-RP02
- Product Quantity:
- 200
- Category:
- -
- Supplier:
- Smart Serology
- Gene target:
- TPO _ THPO Antibody
Related genes to: TPO _ THPO Antibody
- Gene:
- MPL NIH gene
- Name:
- MPL proto-oncogene, thrombopoietin receptor
- Previous symbol:
- -
- Synonyms:
- CD110, TPOR, THPOR
- Chromosome:
- 1p34.2
- Locus Type:
- gene with protein product
- Date approved:
- 1990-09-10
- Date modifiied:
- 2019-04-23
- Gene:
- THPO NIH gene
- Name:
- thrombopoietin
- Previous symbol:
- MGDF
- Synonyms:
- TPO, MPLLG
- Chromosome:
- 3q27.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-11-04
- Date modifiied:
- 2019-04-23
Related products to: TPO _ THPO Antibody
Related articles to: TPO _ THPO Antibody
- Inherited blood disorders (IBDs) are a major health concern in the Kingdom of Saudi Arabia (KSA), largely due to the high prevalence of consanguineous marriages. - Source: PubMed
Publication date: 2026/04/01
Younis Nancy SAlkabsh Rahma MNasser Alqahtani Shahad MAljuail HajerAlhashim Manar ABokhamsin Shahad AAlbaqshi Layla JAlqadhib Salsabil FAldandan Jumanah AAlshakhs Zahra AAltaweel Maryam HMohamed Maged E - The cytokine thrombopoietin (THPO) promotes both self-renewal and cell cycle quiescence of adult bone marrow (BM) hematopoietic stem cells (HSCs). It remains unclear how THPO differentially regulates HSC expansion versus quiescence and whether it influences the broader BM hematopoietic hierarchy, particularly multipotent progenitor cells (MPPs), which express MPL, the receptor for THPO. Adult constitutional Thpo-knockout mice exhibited significant decrease in both HSC and MPP numbers, yet single-cell RNA sequence-based genetic changes were prominent only in HSCs. Induced deletion of Thpo in adult mice showed that THPO primarily maintains adult BM HSC numbers by inhibiting apoptosis. Thpo deficiency-driven reduction of adult BM MPPs was attributed to the shortage of expansion and differentiation of HSCs during neonatal BM hematopoiesis. Drug-mediated enhancement of THPO signaling in neonatal Thpo-deficient mice rescued adult BM progenitor cell numbers but not HSC apoptosis. THPO function is thus limited during adult hematopoiesis but is critical during neonatal development to establish a structured HSC and MPP hierarchy. - Source: PubMed
Publication date: 2026/03/26
Mochizuki-Kashio MakikoYahagi AyanoYokomizo TomomasaUmemoto TerumasaSuda ToshioNakamura-Ishizu Ayako - Hereditary thrombocytosis (HT) is a rare cause of elevated platelet counts in children, most commonly resulting from germline variants in or . We report the first description of bone marrow morphology in a pediatric patient with germline homozygous Baltimore (K39N) variant, a functional polymorphism resulting in HT. The patient had persistent thrombocytosis from infancy without bleeding or thrombotic complications. Bone marrow biopsy demonstrated mild hypocellularity, increased megakaryocytes forming small clusters, and megakaryocytic atypia partially overlapping with the morphologic features of myeloproliferative neoplasms (MPN). However, a somatic cytogenetic or molecular abnormality was not identified and it was determined that the thrombocytosis and bone marrow morphology were driven by the homozygous germline MPL Baltimore variant. Literature review found reports of bone marrow morphology in HT showing varying degrees of megakaryocytic proliferation and atypia with differences seen between specific germline variants. Cases with germline P106L variant have similar morphology as this homozygous Baltimore case. While cases of germline S550N are nearly identical to MPN with more severe megakaryocytic atypia and frequent development of marrow fibrosis. This case underscores the importance of considering HT in children with unexplained thrombocytosis and highlights the diagnostic pitfall of misclassifying HT as MPN. - Source: PubMed
Publication date: 2026/03/21
Kodimyala RoopaBrannock KristinaCampbell AmandaZajo KristinRose Melissa JKaumeyer Benjamin - : Chronic thromboembolic pulmonary hypertension (CTEPH) is a rare disease, in which multiple genetic and environmental factors may contribute. This study aimed to identify potential genetic determinants in patients with CTEPH and to compare their occurrence to a control group, which included patients with pulmonary embolism who had not developed CTEPH. : Tier 1 and 2 genes related to coagulation, fibrinolysis and platelet disorders-as recommended by the International Society on Thrombosis and Haemostasis-and genes associated with vascular conditions were analyzed in n = 15 patients with CTEPH and n = 17 controls using next-generation sequencing. Non-synonymous, rare variants were collected and interpreted. : As expected, no single gene or variant was consistently present among CTEPH patients. Instead, individuals carried different mutations and combinations of variants. We identified several variants that were not found in the control group. Candidate variants were detected in , , , , , , , , , , , , , , , , , , , and We did not detect exclusive variants in , , and although they were suggested as candidates in previous studies. Elevated factor VIII and von Willebrand factor in CTEPH could not be explained by mutations in and . : Our study supports the hypothesis of heterogeneous genetic background in CTEPH, involving multiple pathways such as coagulation, altered fibrinolysis and impaired angiogenesis. These results provide a basis for more detailed investigations into specific genes and variants potentially associated with CTEPH in larger cohorts. - Source: PubMed
Publication date: 2025/11/06
Bereczky ZsuzsannaKolodzey GáborBorsos SaroltaBalogh LászlóBiró Petra ErzsébetMolnár ÉvaRázsó KatalinPéter AndreaBarta JuditSzűk Tibor - Glioma is the most common primary brain tumor in adults, with glioblastoma (GBM) being the most aggressive subtype. The causal relationship between platelet count and glioma risk remains unclear. This study aimed to evaluate this relationship using Mendelian randomization (MR) methodology. - Source: PubMed
Publication date: 2025/11/20
Han XiaoYongChen MengyanJi ZhishengZhang Hui