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Kumi Kawai

Researcher at Nagoya University

Publications -  43
Citations -  2480

Kumi Kawai is an academic researcher from Nagoya University. The author has contributed to research in topics: Glial cell line-derived neurotrophic factor & Tyrosine. The author has an hindex of 25, co-authored 42 publications receiving 2302 citations. Previous affiliations of Kumi Kawai include University of California, Berkeley & Aichi Medical University.

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Akt/PKB Regulates Actin Organization and Cell Motility via Girdin/APE

TL;DR: This work identifies an Akt substrate, designated Girdin/APE (Akt-phosphorylation enhancer), which is an actin binding protein, which plays a crucial role in the formation of stress fibers and lamellipodia.
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Characterization of intracellular signals via tyrosine 1062 in RET activated by glial cell line-derived neurotrophic factor.

TL;DR: It is suggested that the RAS and PI3-K pathways activated by GDNF bifurcate mainly through SHC bound to tyrosine 1062 in RET, which is important for activation of CREB and NF-κB in GDNF-treated cells, respectively.
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A Targeting Mutation of Tyrosine 1062 in Ret Causes a Marked Decrease of Enteric Neurons and Renal Hypoplasia

TL;DR: It is demonstrated that the signal via tyrosine 1062 plays an important role in histogenesis of the enteric nervous system and nephrogenesis.
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The RET proto-oncogene: a molecular therapeutic target in thyroid cancer.

TL;DR: The RET proto‐oncogene and some signaling molecules that function downstream of RET could be potential targets for the development of selective cancer therapeutics.
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Biological and biochemical properties of Ret with kinase domain mutations identified in multiple endocrine neoplasia type 2B and familial medullary thyroid carcinoma

TL;DR: Interestingly, the level of transforming activity correlated with clinical phenotypes; high group RET with the A883F or M918T mutation and low group Ret with the E768D, V804L or S891A mutation were associated with the development of MEN 2B and FMTC, respectively.