Thrombopoietin Antibody [H8L15] | Primary Antibodies

Application: Reactivity: Human

Lane 1: Jurkat

Usage Information

Dilution
WB1:1000-1:5000 IHC1:4000 IF1:50 FCM1:40

Application
WB, IHC, IF, FCM

Reactivity
Human

Source
Rabbit Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW
37 kDa

Datasheet & SDS

Biological Description

Specificity
Thrombopoietin Antibody [H8L15] detects endogenous levels of total Thrombopoietin protein.

Clone
H8L15

Synonym(s)
MGDF; THPO; Thrombopoietin; C‑mpl ligand; Megakaryocyte colony‑stimulating factor; Megakaryocyte growth and development factor; Myeloproliferative leukemia virus oncogene ligand; ML

Background
Thrombopoietin (TPO), the primary hormonal regulator of thrombopoiesis, circulates as a glycoprotein primarily synthesized in the liver and kidney to bind its receptor c-Mpl on megakaryocyte progenitors and hematopoietic stem cells, driving platelet production and stem cell maintenance through tightly controlled feedback. It features a helical cytokine domain that docks into predimerized c-Mpl ectodomains, inducing conformational rearrangement and juxtapositions of intracellular box1 motifs to activate associated JAK2 kinases for cross-phosphorylation at key tyrosines. This unleashes the canonical JAK2-STAT5 signaling axis, where phospho-STAT5 homodimerizes and translocates to induce transcription of MafG and other megakaryocytic genes for polyploidization and proplatelet formation, while parallel activation of PI3K-Akt inhibits FOXO3a to block apoptosis and Shc-Grb2-SOS-ERK fosters proliferation; the pathway branches further through PLCγ-IP3 for calcium mobilization that sustains NF-κB and NFAT for survival. Negative regulation occurs via SOCS proteins and protein phosphatases that dampen JAK2 activity, with platelet mass inversely controlling circulating TPO levels through receptor-mediated uptake and clearance. TPO licenses quiescent HSC self-renewal in osteoblastic niches while committing progenitors to the megakaryocyte lineage, making it indispensable for researchers modeling emergency thrombopoiesis in xenograft assays or dissecting lineage bias via phospho-flow cytometry of STAT5 activation. Deficiency manifests as severe thrombocytopenia and marrow failure, whereas receptor mutations like W515L or JAK2 V617F provoke clonal thrombocytosis in essential thrombocythemia. Its liver-dominant production with skeletal muscle upregulation during regeneration offers tissue-specific interrogation, while recombinant mimetics like romiplostim exploit the pathway therapeutically to normalize counts in immune thrombocytopenia without exhausting stem cell reserves.

Background

Thrombopoietin (TPO), the primary hormonal regulator of thrombopoiesis, circulates as a glycoprotein primarily synthesized in the liver and kidney to bind its receptor c-Mpl on megakaryocyte progenitors and hematopoietic stem cells, driving platelet production and stem cell maintenance through tightly controlled feedback. It features a helical cytokine domain that docks into predimerized c-Mpl ectodomains, inducing conformational rearrangement and juxtapositions of intracellular box1 motifs to activate associated JAK2 kinases for cross-phosphorylation at key tyrosines. This unleashes the canonical JAK2-STAT5 signaling axis, where phospho-STAT5 homodimerizes and translocates to induce transcription of MafG and other megakaryocytic genes for polyploidization and proplatelet formation, while parallel activation of PI3K-Akt inhibits FOXO3a to block apoptosis and Shc-Grb2-SOS-ERK fosters proliferation; the pathway branches further through PLCγ-IP3 for calcium mobilization that sustains NF-κB and NFAT for survival. Negative regulation occurs via SOCS proteins and protein phosphatases that dampen JAK2 activity, with platelet mass inversely controlling circulating TPO levels through receptor-mediated uptake and clearance. TPO licenses quiescent HSC self-renewal in osteoblastic niches while committing progenitors to the megakaryocyte lineage, making it indispensable for researchers modeling emergency thrombopoiesis in xenograft assays or dissecting lineage bias via phospho-flow cytometry of STAT5 activation. Deficiency manifests as severe thrombocytopenia and marrow failure, whereas receptor mutations like W515L or JAK2 V617F provoke clonal thrombocytosis in essential thrombocythemia. Its liver-dominant production with skeletal muscle upregulation during regeneration offers tissue-specific interrogation, while recombinant mimetics like romiplostim exploit the pathway therapeutically to normalize counts in immune thrombocytopenia without exhausting stem cell reserves.

References
https://pubmed.ncbi.nlm.nih.gov/34097561/ https://pubmed.ncbi.nlm.nih.gov/30039510/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%