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美国加州大学伯克利分校2024年招聘博士后(脂、肝代谢生物学)

信息来源:美国加州大学伯克利分校 | 作者:admin | 时间:2024-03-04 10:42

美国加州大学伯克利分校2024年招聘博士后(脂、肝代谢生物学)

加利福尼亚大学伯克利分校(University of California,Berkeley),简称伯克利,坐落美国旧金山湾区伯克利市,是公立研究型大学,被誉为“公立常春藤”,是美国大学协会成员,全球大学校长论坛成员,入选英国政府“高潜力人才签证计划”。

Postdoctoral fellow in metabolic biology on adipose and liver at the Sona Kang Lab, UC Berkeley

Epigenetic and molecular mechanisms of metabolism – Dr. Sona Kang Lab, UC Berkeley

Dive into the intricacies of metabolic regulation by joining the esteemed laboratory of Dr. Sona Kang at the Department of Nutritional Sciences and Toxicology, UC Berkeley. We are actively recruiting a post-doctoral research fellow to contribute to cutting-edge research elucidating the epigenetic and molecular intricacies governing metabolic dysregulation, with a primary focus on identifying therapeutic targets for obesity and type 2 diabetes.

Our lab seeks a highly skilled individual with expertise in molecular and cell biology, metabolic phenotyping of mouse models, and genome-wide profiling studies. The successful candidate will lead projects investigating the pathogenic mechanisms of type 2 diabetes, obesity, and Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) and/or will implement a CRISPR screening project related to adipose metabolism. Elevate your scientific career by applying your expertise to unravel the mysteries of metabolic disorders. Learn more about our research: https://nst.berkeley.edu/users/sona-kang.

Major Publications from Kang Lab:

TET3 plays a critical role in white adipose development and diet-induced remodeling. Cell Reports 2023

AIFM2 is required for high-intensity aerobic exercise by promoting glucose utilization. Diabetes. 2022

JMJD8 is a Novel Molecular Nexus Between Adipocyte-Intrinsic Inflammation and Insulin Resistance Diabetes. 2021

A necessary role of DNMT3A in endurance exercise by suppressing ALDH1L1-mediated oxidative stress. EMBO. 2021

TET1 is a beige adipocyte–selective epigenetic suppressor of thermogenesis. Nat Commun. 2020

TET2 facilitates PPARγ agonist–mediated gene regulation and insulin sensitization in adipocytes. Metabolism. 2018

DNMT3A is an epigenetic mediator of adipose insulin resistance. eLife. 2017

Qualifications:

We are seeking self-motivated and talented applicants with the ability to think critically and excellent interpersonal communication skills.

The successful candidate will lead project(s) requiring technical expertise, such as metabolic characterization of mouse models, cell culture studies, and/or biochemical and molecular studies. Applicants who has expertise in one of the following areas are desirable: molecular and cell biology, metabolic phenotyping of mouse models, and genome-wide profiling studies.

One of the new projects involves investigating the pathogenic mechanisms of metabolic dysfunction-associated steatotic liver disease (MASLD) and CRISPR screening. Individuals with experience in liver biology and CRISPR screening are highly encouraged to apply.

PhD students who are expected to graduate are strongly encouraged to apply for this position.

Interested applicants should directly e-mail Dr. Sona Kang at sonakanglab@gmail.com a single PDF file that includes personal statment and CV and names/contact information of at least three individuals for references.

Salary and Benefits:

This position provides full benefits. Salary will be commensurate with qualifications and experience and based on UC Berkeley salary scale.

TO APPLY

Interested applicants should directly e-mail Dr. Sona Kang at sonakanglab@gmail.com a single PDF file that includes cover letter and CV and contact info of three individuals for references.

Appointment

The initial appointment is for 24 months based upon campus policy, with renewal based on performance and funding. This is a full-time appointment. Salary will be commensurate with qualifications and experience and based on UC Berkeley Postdoc salary scale including benefits. https://www.ucop.edu/academic-personnel-programs/_files/2022-23/april-2023-ase-gsr-postoc-salary-scales/t23.pdf

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