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Phospho-p44/42 MAPK (Erk1/2) (Thr202/Tyr204) (D13.14.4E) XP(tm) Rabbit mAb (Alexa Fluor(R) 488 Conjugate) antibody

RRID:AB_2139960

Antibody ID

AB_2139960

Target Antigen

MAPK3 human, cow, rat, mouse

Proper Citation

(Cell Signaling Technology Cat# 4344, RRID:AB_2139960)

Clonality

monoclonal antibody

Comments

Useful for flow cytometry; The following antibodies were determined to be duplicates and consolidated by curator on 10/2018: AB_10695876, AB_2139960.

Host Organism

rabbit

Vendor

Cell Signaling Technology

Cat Num

4344

Publications that use this research resource

Spred1 Safeguards Hematopoietic Homeostasis against Diet-Induced Systemic Stress.

  • Tadokoro Y
  • Cell Stem Cell
  • 2018 May 3

Literature context:


Abstract:

Stem cell self-renewal is critical for tissue homeostasis, and its dysregulation can lead to organ failure or tumorigenesis. While obesity can induce varied abnormalities in bone marrow components, it is unclear how diet might affect hematopoietic stem cell (HSC) self-renewal. Here, we show that Spred1, a negative regulator of RAS-MAPK signaling, safeguards HSC homeostasis in animals fed a high-fat diet (HFD). Under steady-state conditions, Spred1 negatively regulates HSC self-renewal and fitness, in part through Rho kinase activity. Spred1 deficiency mitigates HSC failure induced by infection mimetics and prolongs HSC lifespan, but it does not initiate leukemogenesis due to compensatory upregulation of Spred2. In contrast, HFD induces ERK hyperactivation and aberrant self-renewal in Spred1-deficient HSCs, resulting in functional HSC failure, severe anemia, and myeloproliferative neoplasm-like disease. HFD-induced hematopoietic abnormalities are mediated partly through alterations to the gut microbiota. Together, these findings reveal that diet-induced stress disrupts fine-tuning of Spred1-mediated signals to govern HSC homeostasis.

Funding information:
  • Arthritis Research UK - 17522(United Kingdom)