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Rabbit Anti-DDDDK Tag Polyclonal Antibody, Unconjugated

RRID:AB_591224

Antibody ID

AB_591224

Target Antigen

DDDDK Tag bovine, canine, chicken/avian, donkey, drosophila, feline, guinea pig, hamster, human, mouse, other, porcine, rabbit, rat, sheep, simian, xenopus, yeast, all

Proper Citation

(MBL International Cat# PM020, RRID:AB_591224)

Clonality

polyclonal antibody

Comments

manufacturer recommendations: Immunocytochemistry; Immunoprecipitation; Western Blot; Western Blot, Immunoprecipitation, Immunocytochemistry

Host Organism

rabbit

Vendor

MBL International

Cat Num

PM020

Publications that use this research resource

NOTCH2 Hajdu-Cheney Mutations Escape SCFFBW7-Dependent Proteolysis to Promote Osteoporosis.

  • Fukushima H
  • Mol. Cell
  • 2017 Nov 16

Literature context: RRID:AB_591224 Monoclonal anti-HA BioLegend Ca


Abstract:

Hajdu-Cheney syndrome (HCS), a rare autosomal disorder caused by heterozygous mutations in NOTCH2, is clinically characterized by acro-osteolysis, severe osteoporosis, short stature, neurological symptoms, cardiovascular defects, and polycystic kidneys. Recent studies identified that aberrant NOTCH2 signaling and consequent osteoclast hyperactivity are closely associated with the bone-related disorder pathogenesis, but the exact molecular mechanisms remain unclear. Here, we demonstrate that sustained osteoclast activity is largely due to accumulation of NOTCH2 carrying a truncated C terminus that escapes FBW7-mediated ubiquitination and degradation. Mice with osteoclast-specific Fbw7 ablation revealed osteoporotic phenotypes reminiscent of HCS, due to elevated Notch2 signaling. Importantly, administration of Notch inhibitors in Fbw7 conditional knockout mice alleviated progressive bone resorption. These findings highlight the molecular basis of HCS pathogenesis and provide clinical insights into potential targeted therapeutic strategies for skeletal disorders associated with the aberrant FBW7/NOTCH2 pathway as observed in patients with HCS.

Funding information:
  • NIMH NIH HHS - R01 MH086920(United States)

TRIB3 Promotes APL Progression through Stabilization of the Oncoprotein PML-RARα and Inhibition of p53-Mediated Senescence.

  • Li K
  • Cancer Cell
  • 2017 May 8

Literature context: CH PM020; RRID:AB_591224 Anti-DDDDK


Abstract:

Acute promyelocytic leukemia (APL) is driven by the oncoprotein PML-RARα, which antagonizes myeloid differentiation and promotes APL-initiating cell self-renewal. Combined all-trans retinoic acid (ATRA) with arsenic trioxide (As2O3) or chemotherapy dramatically improves the prognosis of APL patients. Here we report that expression of pseudokinase Tribble 3 (TRIB3) associates positively with APL progression and therapeutic resistance. The elevated TRIB3 expression promotes APL by interacting with PML-RARα and suppressing its sumoylation, ubiquitylation, and degradation. This represses PML nuclear body assembly, p53-mediated senescence, and cell differentiation, and supports cellular self-renewal. Genetically inhibiting TRIB3 expression or combination of a peptide disturbing TRIB3/PML-RARα interaction with ATRA/As2O3 eradicates APL by accelerating PML-RARα degradation. Our study provides insight into APL pathogenesis and a potential therapeutic option against APL.