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「"Sheikh BN "[Author]」の検索結果

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Vascular Homeostasis and Inflammation in Health and Disease-Lessons from Single Cell Technologies.

Neural metabolic imbalance induced by MOF dysfunction triggers pericyte activation and breakdown of vasculature.

Evolutionary conserved NSL complex/BRD4 axis controls transcription activation via histone acetylation.

Systematic Identification of Cell-Cell Communication Networks in the Developing Brain.

The non-specific lethal (NSL) complex at the crossroads of transcriptional control and cellular homeostasis.

PHF6 regulates hematopoietic stem and progenitor cells and its loss synergizes with expression of TLX3 to cause leukemia.

The many lives of KATs - detectors, integrators and modulators of the cellular environment.

Subtle Changes in the Levels of BCL-2 Proteins Cause Severe Craniofacial Abnormalities.

Inhibitors of histone acetyltransferases KAT6A/B induce senescence and arrest tumour growth.

MOZ and BMI1 act synergistically to maintain Hematopoietic Stem Cells.

MOZ (KAT6A) is essential for the maintenance of classically defined adult hematopoietic stem cells.

Cortical Layer Inversion and Deregulation of Reelin Signaling in the Absence of SOCS6 and SOCS7.

MOF maintains transcriptional programs regulating cellular stress response.

MOZ and BMI1 play opposing roles during Hox gene activation in ES cells and in body segment identity specification in vivo.

MOZ (MYST3, KAT6A) inhibits senescence via the INK4A-ARF pathway.

MOZ regulates B cell progenitors and, consequently, Moz haploinsufficiency dramatically retards MYC-induced lymphoma development.

Excessive versus Physiologically Relevant Levels of Retinoic Acid in Embryonic Stem Cell Differentiation.

Crafting the brain - role of histone acetyltransferases in neural development and disease.

MOZ Regulates the Tbx1 Locus, and Moz Mutation Partially Phenocopies DiGeorge Syndrome.

Querkopf is a key marker of self-renewal and multipotency of adult neural stem cells.

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