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Myogenin antibody

RRID:AB_2250893

Antibody ID

AB_2250893

Target Antigen

Myogenin

Proper Citation

(Agilent Cat# M3559, RRID:AB_2250893)

Clonality

monoclonal antibody

Comments

Used By NYUIHC-1385. Original Manufacturer: Dako. Now part of Agilent.

Clone ID

F5D

Host Organism

mouse

Vendor

Agilent

Cat Num

M3559

Publications that use this research resource

Hedgehog Pathway Drives Fusion-Negative Rhabdomyosarcoma Initiated From Non-myogenic Endothelial Progenitors.

  • Drummond CJ
  • Cancer Cell
  • 2018 Jan 8

Literature context:


Abstract:

Rhabdomyosarcoma (RMS) is a pediatric soft tissue sarcoma that histologically resembles embryonic skeletal muscle. RMS occurs throughout the body and an exclusively myogenic origin does not account for RMS occurring in sites devoid of skeletal muscle. We previously described an RMS model activating a conditional constitutively active Smoothened mutant (SmoM2) with aP2-Cre. Using genetic fate mapping, we show SmoM2 expression in Cre-expressing endothelial progenitors results in myogenic transdifferentiation and RMS. We show that endothelium and skeletal muscle within the head and neck arise from Kdr-expressing progenitors, and that hedgehog pathway activation results in aberrant expression of myogenic specification factors as a potential mechanism driving RMS genesis. These findings suggest that RMS can originate from aberrant development of non-myogenic cells.

Funding information:
  • NCI NIH HHS - K08 CA151649()
  • NCI NIH HHS - P30 CA021765()
  • NCI NIH HHS - R01 CA216344()
  • NIAID NIH HHS - R21AI094333(United States)

Klf5 regulates muscle differentiation by directly targeting muscle-specific genes in cooperation with MyoD in mice.

  • Hayashi S
  • Elife
  • 2016 Oct 15

Literature context:


Abstract:

Kr├╝ppel-like factor 5 (Klf5) is a zinc-finger transcription factor that controls various biological processes, including cell proliferation and differentiation. We show that Klf5 is also an essential mediator of skeletal muscle regeneration and myogenic differentiation. During muscle regeneration after injury (cardiotoxin injection), Klf5 was induced in the nuclei of differentiating myoblasts and newly formed myofibers expressing myogenin in vivo. Satellite cell-specific Klf5 deletion severely impaired muscle regeneration, and myotube formation was suppressed in Klf5-deleted cultured C2C12 myoblasts and satellite cells. Klf5 knockdown suppressed induction of muscle differentiation-related genes, including myogenin. Klf5 ChIP-seq revealed that Klf5 binding overlaps that of MyoD and Mef2, and Klf5 physically associates with both MyoD and Mef2. In addition, MyoD recruitment was greatly reduced in the absence of Klf5. These results indicate that Klf5 is an essential regulator of skeletal muscle differentiation, acting in concert with myogenic transcription factors such as MyoD and Mef2.