Regot相关文献与解析，生知库 | 链接生命科学的每一步

Sinha Niladri K, McKenney Connor, Yeow Zhong Y, Li Jeffrey J, Nam Ki Hong, Yaron-Barir Tomer M, Johnson Jared L, Huntsman Emily M, Cantley Lewis C, Ordureau Alban, Regot Sergi, Green Rachel

细胞生物学

氧化应激

发表日期：2024

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Oncogenic Kras induces spatiotemporally specific tissue deformation through converting pulsatile into sustained ERK activation.

致癌 Kras 通过将脉冲式 ERK 激活转化为持续性 ERK 激活，诱导时空特异性的组织变形

期刊:Nature Cell Biology

影响因子:19.1

doi:10.1038/s41556-024-01413-y

Xin Tianchi, Gallini Sara, Wei Haoyang, Gonzalez David G, Matte-Martone Catherine, Machida Hiroki, Fujiwara Hironobu, Pasolli H Amalia, Suozzi Kathleen C, Gonzalez Lauren E, Regot Sergi, Greco Valentina

肿瘤

发表日期：2024

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Sustained ERK signaling promotes G2 cell cycle exit and primes cells for whole-genome duplication

持续的ERK信号传导促进G2期细胞周期退出，并使细胞做好全基因组复制的准备。

期刊:Developmental Cell

影响因子:10.7

doi:10.1016/j.devcel.2024.03.032

Adler Guerrero Zuniga ,Timothy J Aikin ,Connor McKenney ,Yovel Lendner ,Alain Phung ,Paul W Hook ,Amy Meltzer ,Winston Timp ,Sergi Regot

Organ function is preserved despite reorganization of niche architecture in the hair follicle

尽管毛囊中的生态位结构发生重组，器官功能仍得以保留

期刊:Cell Stem Cell

影响因子:19.8

doi:10.1016/j.stem.2023.06.003

Haoyang Wei, Shuangshuang Du, Jeeun Parksong, H Amalia Pasolli, Catherine Matte-Martone, Sergi Regot, Lauren E Gonzalez, Tianchi Xin, Valentina Greco

信号转导

发表日期：2023

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Systematic analysis of the MAPK signaling network reveals MAP3K-driven control of cell fate

MAPK 信号网络的系统分析揭示了 MAP3K 驱动的细胞命运控制

期刊:Cell Systems

影响因子:9

doi:10.1016/j.cels.2022.10.003

Amy F Peterson, Kayla Ingram, E J Huang, Jeeun Parksong, Connor McKenney, Gabriel S Bever, Sergi Regot

CaMKII oxidation is a critical performance/disease trade-off acquired at the dawn of vertebrate evolution

CaMKII氧化是脊椎动物进化初期获得的一种关键的性能/疾病权衡。

期刊:Nature Communications

影响因子:14.7

doi:10.1038/s41467-021-23549-3

Qinchuan Wang ，Erick O Hernández-Ochoa ，Meera C Viswanathan ，Ian D Blum ，Danh C Do ，Jonathan M Granger ，Kevin R Murphy ，An-Chi Wei ，Susan Aja ，Naili Liu ，Corina M Antonescu ，Liliana D Florea ，C Conover Talbot Jr ，David Mohr ，Kathryn R Wagner ，Sergi Regot ，Richard M Lovering ，Peisong Gao ，Mario A Bianchet ，Mark N Wu ，Anthony Cammarato ，Martin F Schneider ，Gabriel S Bever ，Mark E Anderson

发表日期：2021

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Mechanisms of whole-genome doubling in cancer evolution

癌症进化中全基因组加倍的机制

Cell cycle regulation by the ribotoxic stress response

核糖体毒性应激反应对细胞周期的调控

CDK2 activity crosstalk on the ERK kinase translocation reporter can be resolved computationally

CDK2活性对ERK激酶易位报告基因的串扰可以通过计算方法解析。

CDK4/6 activity is required during G(2) arrest to prevent stress-induced endoreplication.

CDK4/6 活性在 G(2) 阻滞期间是必需的，以防止应激诱导的内复制

The ribotoxic stress response drives UV-mediated cell death.

核糖体毒性应激反应驱动紫外线介导的细胞死亡

Oncogenic Kras induces spatiotemporally specific tissue deformation through converting pulsatile into sustained ERK activation.

致癌 Kras 通过将脉冲式 ERK 激活转化为持续性 ERK 激活，诱导时空特异性的组织变形

Sustained ERK signaling promotes G2 cell cycle exit and primes cells for whole-genome duplication

持续的ERK信号传导促进G2期细胞周期退出，并使细胞做好全基因组复制的准备。

Organ function is preserved despite reorganization of niche architecture in the hair follicle

尽管毛囊中的生态位结构发生重组，器官功能仍得以保留

Systematic analysis of the MAPK signaling network reveals MAP3K-driven control of cell fate

MAPK 信号网络的系统分析揭示了 MAP3K 驱动的细胞命运控制

CaMKII oxidation is a critical performance/disease trade-off acquired at the dawn of vertebrate evolution

CaMKII氧化是脊椎动物进化初期获得的一种关键的性能/疾病权衡。