Insulin Signaling And Receptor Cross Talk (R01) | Apply Online

Opportunity Summary:

The Insulin Signaling And Receptor Cross Talk (R01) opportunity (Funding Opportunity Number PA-07-058) is an NIH investigator-initiated research grant announcement sponsored by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) together with the National Institute on Aging (NIA). It is set up to support R01 projects that dig into how insulin signaling works in real biological settings where the insulin receptor does not operate alone, but instead interacts with other receptors and signaling networks. The central theme is "crosstalk": the molecular, cellular, and whole-body communication that shapes insulin responses within a tissue and across multiple insulin-responsive tissues.

The scientific purpose of the announcement is to stimulate new and innovative research on the fundamental mechanisms of insulin receptor action in target tissues when other cellular receptors and pathways are also engaged. In practical terms, the FOA is pushing applicants to move beyond simplified, single-pathway models and instead explain how insulin signaling is integrated with other inputs (for example, growth factor receptors, cytokine and inflammatory signaling, nutrient-sensing pathways, stress pathways, and other receptor-mediated systems). A key goal is to broaden understanding of how insulin signals coordinate responses between tissues, recognizing that insulin action is distributed and interdependent across organs such as liver, skeletal muscle, adipose tissue, pancreas, and potentially the brain and vasculature, depending on the research focus.

A major emphasis is the relevance of these signaling interactions to disease. The announcement specifically highlights interest in how insulin receptor crosstalk and pathway integration may influence the development and/or progression of diabetes and its complications. That includes the idea that abnormal signaling interactions can contribute to insulin resistance, beta cell dysfunction, dysregulated glucose and lipid metabolism, and downstream complications. Projects responsive to this FOA would typically aim to clarify mechanisms that explain why insulin action fails in certain physiological or pathological states, how compensatory pathways arise, and how inter-tissue signaling coordination breaks down in ways that promote disease.

Administratively, this is a discretionary grant program using the NIH R01 funding instrument and falls under the health funding activity category. It is associated with CFDA numbers 93.847 (Diabetes, Digestive, and Kidney Diseases Extramural Research) and 93.866 (Aging Research), reflecting the partnership between NIDDK and NIA and the relevance of insulin signaling both to metabolic disease and to aging biology. The opportunity does not require cost sharing or matching. The FOA used multiple receipt dates (rather than a single deadline), meaning applicants could submit on standard NIH cycle dates while the announcement was active.

Eligibility is broad and includes many types of domestic organizations such as public and private institutions of higher education, nonprofit organizations (including those with and without 501(c)(3) status), small businesses and other for-profit organizations, state and local governments (including counties, cities, townships, special districts), independent school districts, public housing authorities/Indian housing authorities, and Native American tribal governments and tribal organizations. Importantly, the announcement also states that foreign institutions are eligible to apply, eligible federal government agencies may apply, and faith-based or community-based organizations may apply as well, provided they meet NIH requirements.

The original posting date was November 20, 2006, with an archive date of June 1, 2009. The full announcement was hosted on the NIH grants site (link provided in the source data). For technical issues accessing or linking to the FOA, the contact listed is the NIH Office of Extramural Research (OER) webmaster via FBOWebmaster@OD.NIH.GOV.

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