tbuckley/cabot-search huggingface dataset:
Phase 2 Study of Palbociclib in Patients with Tumors with CDK4 or CDK6 Amplification: Results from the NCI-MATCH ECOG-ACRIN Trial (EAY131) Sub-protocol Z1C
Authors: Mark H. O'Hara, Opeyemi Jegede, Mark A. Dickson, Angela M. DeMichele, Richard Piekarz, Robert J. Gray, Victoria Wang, Lisa M. McShane, Lawrence V. Rubinstein, David R. Patton, P. Mickey Williams, Stanley R. Hamilton, Adedayo Onitilo, James V. Tricoli, Barbara A. Conley, Carlos L. Arteaga, Lyndsay N. Harris, Peter J. O'Dwyer, Alice P. Chen, Keith T. Flaherty
Journal: Clinical Cancer Research (2024)

Amplification of cyclin-dependent kinase 4 (CDK4) and CDK6 is a feature of a variety of malignancies, and preclinical evidence suggests that inhibition of CDK4/6 is a plausible treatment strategy in these tumors. Subprotocol Z1C of the NCI-Molecular Analysis for Therapy Choice trial was designed to evaluate the CDK4/6 inhibitor palbociclib in CDK4- or CDK6-amplified tumors.
Data- and Physics-driven Deep Learning Based Reconstruction for Fast MRI: Fundamentals and Methodologies
Authors: Jiahao Huang, Yinzhe Wu, Fanwen Wang, Yingying Fang, Yang Nan, Cagan Alkan, Daniel Abraham, Congyu Liao, Lei Xu, Zhifan Gao, Weiwen Wu, Lei Zhu, Zhaolin Chen, Peter Lally, Neal Bangerter, Kawin Setsompop, Yike Guo, Daniel Rueckert, Ge Wang, Guang Yang
Journal: IEEE Reviews in Biomedical Engineering (2024)

Magnetic Resonance Imaging (MRI) is a pivotal clinical diagnostic tool, yet its extended scanning times often compromise patient comfort and image quality, especially in volumetric, temporal and quantitative scans. This review elucidates recent advances in MRI acceleration via data and physics-driven models, leveraging techniques from algorithm unrolling models, enhancement-based methods, and plug-and-play models to the emerging full spectrum of generative model-based methods. We also explore the synergistic integration of data models with physics-based insights, encompassing the advancements in multi-coil hardware accelerations like parallel imaging and simultaneous multi-slice imaging, and the optimization of sampling patterns. We then focus on domain-specific challenges and opportunities, including image redundancy exploitation, image integrity, evaluation metrics, data heterogeneity, and model generalization. This work also discusses potential solutions and future research directions, with an emphasis on the role of data harmonization and federated learning for further improving the general applicability and performance of these methods in MRI reconstruction.
Building machines that learn and think with people
Authors: Katherine M. Collins, Ilia Sucholutsky, Umang Bhatt, Kartik Chandra, Lionel Wong, Mina Lee, Cedegao E. Zhang, Tan Zhi-Xuan, Mark Ho, Vikash Mansinghka, Adrian Weller, Joshua B. Tenenbaum, Thomas L. Griffiths
Journal: Nature Human Behaviour (2024)
Risks and protective measures for synthetic relationships
Authors: Christopher Starke, Alfio Ventura, Clara Bersch, Meeyoung Cha, Claes de Vreese, Philipp Doebler, Mengchen Dong, Nicole Krämer, Margarita Leib, Jochen Peter, Lea Schäfer, Ivan Soraperra, Jessica Szczuka, Erik Tuchtfeld, Rebecca Wald, Nils Köbis
Journal: Nature Human Behaviour (2024)
Chinese Expert Consensus on the Whole-Course Management of Hepatocellular Carcinoma (2023 Edition)
Authors: Yu Yang, Juxian Sun, Jianqiang Cai, Minshan Chen, Chaoliu Dai, Tianfu Wen, Jinglin Xia, Mingang Ying, Zhiwei Zhang, Xuewen Zhang, Chihua Fang, Feng Shen, Ping An, Qingxian Cai, Jingyu Cao, Zhen Zeng, Gang Chen, Juan Chen, Ping Chen, Yongshun Chen, Yunfeng Shan, Shuangsuo Dang, Wei-Xing Guo, Jiefeng He, Heping Hu, Bin Huang, Weidong Jia, Kexiang Jiang, Yan Jin, Yongdong Jin, Yun Jin, Gong Li, Yun Liang, Enyu Liu, Hao Liu, Wei Peng, Zhenwei Peng, Zhiyi Peng, Yeben Qian, Wanhua Ren, Jie Shi, Yusheng Song, Min Tao, Jun Tie, Xueying Wan, Bin Wang, Jin Wang, Kai Wang, Kang Wang, Xin Wang, Wenjing Wei, Fei-Xiang Wu, Bangde Xiang, Lin Xie, Jianming Xu, Mao-Lin Yan, Yufu Ye, Jinbo Yue, Xiaoxun Zhang, Yu Zhang, Aibin Zhang, Haitao Zhao, Weifeng Zhao, Xin Zheng, Hongkun Zhou, Huabang Zhou, Jun Zhou, Xinmin Zhou, Shu-Qun Cheng, Qiu Li
Journal: Liver Cancer (2024)

Background: Hepatocellular carcinoma (HCC) is one of the most common malignant tumors in China. Most HCC patients have the complications of chronic liver disease and need overall consideration and whole-course management, including diagnosis, treatment, and follow-up. To develop a reasonable, long-term, and complete management plan, multiple factors need to be considered, including the patient’s general condition, basic liver diseases, tumor stage, tumor biological characteristics, treatment requirements, and economic cost. Summary: To better guide the whole-course management of HCC patients, the Chinese Association of Liver Cancer and the Chinese Medical Doctor Association has gathered multidisciplinary experts and scholars in relevant fields to formulate the “Chinese Expert Consensus on The Whole-Course Management of Hepatocellular Carcinoma (2023).” Key Messages: This expert consensus, based on the current clinical evidence and experience, proposes surgical and nonsurgical HCC management pathways and involves 18 recommendations, including perioperative treatment, systematic treatment combined with local treatment, conversion treatment, special population management, symptomatic support treatment, and follow-up management.
Risk of Infection in Older Adults With Type 2 Diabetes With Relaxed Glycemic Control
Authors: Kasia J. Lipska, Lisa K. Gilliam, Catherine Lee, Jennifer Y. Liu, Vincent X. Liu, Howard H. Moffet, Melissa M. Parker, Heidi Zapata, Andrew J. Karter
Journal: Diabetes Care (2024)

OBJECTIVE To compare the risk of hospitalization for infection among patients who achieve intensive versus relaxed glycemic control. RESEARCH DESIGN AND METHODS This retrospective cohort study included adults age ≥65 years with type 2 diabetes from an integrated health care delivery system. Negative binomial models were used to estimate incidence rates and relative risk (RR) of hospitalization for infections (respiratory; genitourinary; skin, soft tissue, and bone; and sepsis), comparing two levels of relaxed (hemoglobin A1c [HbA1c] 7% to &amp;lt;8% and 8% to &amp;lt;9%) with intensive (HbA1c 6% to &amp;lt;7%) glycemic control from 1 January 2019 to 1 March 2020. RESULTS Among 103,242 older patients (48.5% with HbA1c 6% to &amp;lt;7%, 35.3% with HbA1c 7% to &amp;lt;8%, and 16.1% with HbA1c 8% to &amp;lt;9%), the rate of hospitalization for infections was 51.3 per 1,000 person-years. Compared with HbA1c 6% to &amp;lt;7%, unadjusted risk of hospitalization for infections was significantly elevated among patients with HbA1c 8% to &amp;lt;9% (RR 1.25; 95% CI 1.13, 1.39) but not among patients with HbA1c 7% to &amp;lt;8% (RR 0.99; 95% CI 0.91, 1.08), and the difference became nonsignificant after adjustment. Across categories of infections, the adjusted RR of hospitalization was significantly higher among patients with HbA1c 8% to &amp;lt;9% only for skin, soft tissue, and bone infection (RR 1.33; 95% CI 1.05, 1.69). CONCLUSIONS Older patients with type 2 diabetes who achieve relaxed glycemic control levels endorsed by clinical guidelines are not at significantly increased risk of hospitalization for most infections, but HbA1c 8% to &amp;lt;9% is associated with an increased risk of hospitalization for skin, soft tissue, and bone infections.
DNA-PK inhibition enhances neoantigen diversity and increases T cell responses to immunoresistant tumors
Authors: Allison Joy Nielsen, Gabriella Kyra Albert, Amelia Sanchez, Jiangli Chen, Jing Liu, Andres Sebastian Davalos, Degui Geng, Xander G. Bradeen, Jennifer D. Hintzsche, William Robinson, Martin McCarter, Carol M. Amato, Richard Tobin, Kasey L. Couts, Breelyn Ann Wilky, Eduardo Davila
Journal: Journal of Clinical Investigation (2024)

Effective antitumor T cell activity relies on the expression and MHC presentation of tumor neoantigens. Tumor cells can evade T cell detection by silencing the transcription of antigens or by altering MHC machinery resulting in inadequate neoantigen-specific T cell activation. We identified DNA-PK inhibitor (DNA-PKi) NU7441 as a promising immunomodulator that reduced immunosuppressive proteins while increasing MHC-I expression in a panel of human melanoma cell lines. In tumor-bearing mice, combination therapy using NU7441 and immune adjuvants STING ligand and CD40 agonist (NU-SL40) substantially increased and diversified the neoantigen landscape, antigen presenting machinery, and consequently substantially increased both the number and repertoire of neoantigen-reactive tumor infiltrating lymphocytes (TILs). DNA-PK-inhibition or knockout promoted transcription and protein expression of various neoantigens in human and mouse melanomas and induced sensitivity to ICB in resistant tumors. In patients, PRKDC levels inversely correlated with MHC I expression and CD8 TILs but positively correlated with increased neoantigen loads and improved responses to ICB. These studies suggest that inhibiting DNA-PK activity can restore tumor immunogenicity by increasing neoantigen expression and presentation and broadening the neoantigen-reactive T cell population.
MOGAT3-Mediated DAG Accumulation Drives Acquired Resistance to Anti-BRAF/EGFR Therapy in BRAFV600E-Mutant Metastatic Colorectal Cancer
Authors: Jiawei Wang, Huogang Wang, Wei Zhou, Xin Luo, Huijuan Wang, Qing Meng, Jiaxin Chen, Xiaoyu Chen, Yinqiang Liu, David W. Chan, Zhenyu Ju, Zhangfa Song
Journal: Journal of Clinical Investigation (2024)

BRAFV600E-mutant metastatic colorectal cancer (mCRC) is associated with poor prognosis. The combination of anti-BRAF/EGFR (encorafenib/cetuximab) treatment for patients with BRAFV600E-mutant mCRC improved clinical benefits; unfortunately, inevitable acquired resistance limits the treatment outcome, and the mechanism has not been validated. Here, we discovered that monoacylglycerol O-Acyltransferase 3 (MOGAT3) mediated diacylglycerol (DAG) accumulation contributed to acquired resistance to encorafenib/cetuximab by dissecting BRAFV600E-mutant mCRC patient-derived xenograft (PDX) model exposed to encorafenib/cetuximab administration. Mechanistically, upregulated MOGAT3 promotes DAG synthesis and reduces fatty acid oxidation (FAO)-promoting DAG accumulation and activating PKCα-CRAF-MEK-ERK, driving acquired resistance. Resistance-induced hypoxia promotes MOGAT3 transcriptional elevation; simultaneously, MOGAT3-mediated DAG accumulation increases HIF1A expression in translation level through PKCα-CRAF-eIF4E activation, strengthening the resistance status. Intriguingly, reducing intratumoral DAG by fenofibrate or Pf-06471553 restores the antitumor efficacy of encorafenib/cetuximab on resistant BRAFV600E-mutant mCRC, interrupted PKCα-CRAF-MEK-ERK signaling. These findings reveal the critical metabolite DAG as a modulator of encorafenib/cetuximab efficacy in BRAFV600E-mutant mCRC, suggesting that fenofibrate may prove beneficial for resistant BRAFV600E-mutant mCRC patients.
Combined HDAC8 and checkpoint kinase inhibition induces tumor-selective synthetic lethality in preclinical models
Authors: Ting-Yu Chang, Yan Yan, Zih-Yao Yu, Moeez Rathore, Nian-Zhe Lee, Hui-Ju Tseng, Li-Hsin Cheng, Wei-Jan Huang, Wei Zhang, Ernest R. Chan, Yulan Qing, Ming-Lun Kang, Rui Wang, Kelvin K. Tsai, John J. Pink, William E. Harte, Stanton L. Gerson, Sung-Bau Lee
Journal: Journal of Clinical Investigation (2024)

The elevated level of replication stress is an intrinsic characteristic of cancer cells. Targeting the mechanisms that maintain genome stability to further increase replication stress and thus induce severe genome instability has become a promising approach for cancer treatment. Here, we identify histone deacetylase 8 (HDAC8) as a drug target whose inactivation synergizes with the inhibition of checkpoint kinases to elicit substantial replication stress and compromise genome integrity selectively in cancer cells. We showed that simultaneous inhibition of HDAC8 and checkpoint kinases led to extensive replication fork collapse, irreversible cell-cycle arrest, and synergistic vulnerability in various cancer cells. The efficacy of the combination treatment was further validated in patient tumor-derived organoid (PDO) and xenograft mouse (PDX) models, providing important insights into patient-specific drug responses. Our data revealed that HDAC8 activity was essential for reducing the acetylation level of structural maintenance of chromosomes protein 3 (SMC3) ahead of replication forks and preventing R loop formation. HDAC8 inactivation resulted in slowed fork progression and checkpoint kinase activation. Our findings indicate that HDAC8 guards the integrity of the replicating genome, and the cancer-specific synthetic lethality between HDAC8 and checkpoint kinases provides a promising replication stress-targeting strategy for treating a broad range of cancers.
FoxO1/Rictor axis induces a non-genetic adaptation to Ibrutinib via Akt activation in chronic lymphocytic leukemia
Authors: Laura Ondrisova, Vaclav Seda, Krystof Hlavac, Petra Pavelkova, Eva Hoferkova, Giorgia Chiodin, Lenka Kostalova, Gabriela Mladonicka Pavlasova, Daniel Filip, Josef Vecera, Pedro Faria Zeni, Jan Oppelt, Zuzana Kahounova, Rachel Vichova, Karel Soucek, Anna Panovska, Karla Plevova, Sarka Pospisilova, Martin Simkovic, Filip Vrbacky, Daniel Lysak, Stacey M. Fernandes, Matthew S. Davids, Alba Maiques-Diaz, Stella Charalampopoulou, Jose I. Martin-Subero, Jennifer R. Brown, Michael Doubek, Francesco Forconi, Jiri Mayer, Marek Mraz
Journal: Journal of Clinical Investigation (2024)

BTK inhibitor therapy induces peripheral blood lymphocytosis in chronic lymphocytic leukemia (CLL) lasting for several months. It remains unclear whether non-genetic adaptation mechanisms exist, allowing CLL cells' survival during BTK inhibitor-induced lymphocytosis and/or playing a role in therapy resistance. We show that in approximately 70 % of CLL cases, ibrutinib treatment in vivo increases Akt activity above pre-therapy levels within several weeks, leading to compensatory CLL cell survival and a more prominent lymphocytosis on therapy. Ibrutinib-induced Akt phosphorylation (pAktS473) is caused by the upregulation of FoxO1 transcription factor, which induces expression of Rictor, an assembly protein for mTORC2 protein complex that directly phosphorylates Akt at serine 473 (S473). Knock-out or inhibition of FoxO1 or Rictor led to a dramatic decrease in Akt phosphorylation and growth disadvantage for malignant B cells in the presence of ibrutinib (or PI3K inhibitor idelalisib) in vitro and in vivo. FoxO1/Rictor/pAktS473 axis represents an early non-genetic adaptation to BCR inhibitor therapy not requiring PI3Kδ or BTK kinase activity. We further demonstrate that FoxO1 can be targeted therapeutically, and its inhibition induces CLL cells' apoptosis alone or in combination with BTK inhibitors (ibrutinib, acalabrutinib, pirtobrutinib) and blocks their proliferation triggered by T-cell factors (CD40L, IL-4, and IL-21).
Sialylated glycoproteins suppress immune cell killing by binding to Siglec-7 and Siglec-9 in prostate cancer
Authors: Ru M. Wen, Jessica C. Stark, G. Edward W. Marti, Zenghua Fan, Aram Lyu, Fernando Jose Garcia Marques, Xiangyue Zhang, Nicholas M. Riley, Sarah M. Totten, Abel Bermudez, Rosalie Nolley, Hongjuan Zhao, Lawrence Fong, Edgar G. Engleman, Sharon J. Pitteri, Carolyn R. Bertozzi, James D. Brooks
Journal: Journal of Clinical Investigation (2024)

Prostate cancer is the second leading cause of male cancer death in the U.S. Current immune checkpoint inhibitor-based immunotherapies have improved survival for many malignancies; however, they have failed to prolong survival for prostate cancer. Siglecs (sialic acid-binding immunoglobulin-like lectins) are expressed on immune cells and regulate immune responses and function. Siglec-7 and Siglec-9 contribute to immune evasion by interacting with their ligands. However, the role of Siglec-7/9 receptors and their ligands in prostate cancer remains poorly understood. Here, we find that Siglec-7 and Siglec-9 are associated with poor prognosis in prostate cancer patients, and are highly expressed in myeloid cells, including macrophages, in prostate tumor tissues. Siglecs-7 and -9 ligands were expressed in prostate cancer cells and human prostate tumor tissues. Blocking the interactions between Siglec-7/9 and sialic acids inhibited prostate cancer xenograft growth and increased immune cell infiltration in humanized mice in vivo. Using a CRISPRi screen and mass spectrometry, we identified CD59 as a candidate Siglec-9 ligand in prostate cancer. The identification of Siglecs-7 and -9 as potential therapeutic targets, including CD59/Siglec-9 axis, opens up opportunities for immune-based interventions in prostate cancer.
Distinct mechanisms drive divergent phenotypes in hypertrophic and dilated cardiomyopathy associated TPM1 variants
Authors: Saiti S. Halder, Michael J. Rynkiewicz, Lynne Kim, Meaghan Barry, Ahmed G.A. Zied, Lorenzo R. Sewanan, Jonathan A. Kirk, Jeffrey R. Moore, William Lehman, Stuart G. Campbell
Journal: Journal of Clinical Investigation (2024)

Hypertrophic and dilated cardiomyopathies (HCM and DCM, respectively) are inherited disorders that may be caused by mutations to the same sarcomeric protein but have completely different clinical phenotypes. The precise mechanisms by which point mutations within the same gene bring about phenotypic diversity remain unclear. Our objective has been to develop a mechanistic explanation of diverging phenotypes in two TPM1 mutations, E62Q (HCM) and E54K (DCM). Drawing on data from the literature and experiments with stem cell-derived cardiomyocytes expressing the TPM1 mutations of interest, we constructed computational simulations that provide plausible explanations of the distinct muscle contractility caused by each variant. In E62Q, increased calcium sensitivity and hypercontractility was explained most accurately by a reduction in effective molecular stiffness of tropomyosin and alterations in its interactions with the actin thin filament that favor the 'closed' regulatory state. By contrast, the E54K mutation appeared to act via long-range allosteric interactions to increase the association rate of the C-terminal troponin I mobile domain to tropomyosin/actin. These mutation-linked molecular events produced diverging alterations in gene expression that can be observed in human engineered heart tissues. Modulators of myosin activity confirmed our proposed mechanisms by rescuing normal contractile behavior in accordance with predictions.
Attenuated kidney oxidative metabolism in young adults with type 1 diabetes
Authors: Ye Ji Choi, Gabriel Richard, Guanshi Zhang, Jeffrey B. Hodgin, Dawit S. Demeke, Yingbao Yang, Jennifer A. Schaub, Ian M. Tamayo, Bhupendra K. Gurung, Abhijit S. Naik, Viji Nair, Carissa Birznieks, Alexis MacDonald, Phoom Narongkiatikhun, Susan Gross, Lynette Driscoll, Maureen Flynn, Kalie Tommerdahl, Kristen J. Nadeau, Viral N. Shah, Tim Vigers, Janet K. Snell-Bergeon, Jessica Kendrick, Daniel H. van Raalte, Lu-Ping Li, Pottumarthi Prasad, Patricia Ladd, Bennett B. Chin, David Z. Cherney, Phillip J. McCown, Fadhl Alakwaa, Edgar A. Otto, Frank C. Brosius, Pierre Jean Saulnier, Victor G. Puelles, Jesse A. Goodrich, Kelly Street, Manjeri A. Venkatachalam, Aaron Ruiz, Ian H. de Boer, Robert G. Nelson, Laura Pyle, Denis P. Blondin, Kumar Sharma, Matthias Kretzler, Petter Bjornstad
Journal: Journal of Clinical Investigation (2024)

BACKGROUND. In type 1 diabetes (T1D), impaired insulin sensitivity may contribute to the development of diabetic kidney disease (DKD) through alterations in kidney oxidative metabolism.
Publisher Correction: Rare variant analyses in 51,256 type 2 diabetes cases and 370,487 controls reveal the pathogenicity spectrum of monogenic diabetes genes
Authors: Alicia Huerta-Chagoya, Philip Schroeder, Ravi Mandla, Jiang Li, Lowri Morris, Maheak Vora, Ahmed Alkanaq, Dorka Nagy, Lukasz Szczerbinski, Jesper G. S. Madsen, Silvia Bonàs-Guarch, Fanny Mollandin, Joanne B. Cole, Bianca Porneala, Kenneth Westerman, Josephine H. Li, Toni I. Pollin, Jose C. Florez, Anna L. Gloyn, David J. Carey, Inês Cebola, Uyenlinh L. Mirshahi, Alisa K. Manning, Aaron Leong, Miriam Udler, Josep M. Mercader
Journal: Nature Genetics (2024)
Prevalence of Unrecognized Cognitive Impairment in Federally Qualified Health Centers
Authors: Ambar Kulshreshtha, Erik S. Parker, Nicole R. Fowler, Diana Summanwar, Zina Ben Miled, Arthur H. Owora, James E. Galvin, Malaz A. Boustani
Journal: JAMA Network Open (2024)

There is a need for early and equitable detection of cognitive impairment among older adults.
Glucagon-like peptide-1 receptor agonists before upper gastrointestinal endoscopy and risk of pulmonary aspiration or discontinuation of procedure: cohort study
Authors: Wajd Alkabbani, Karine Suissa, Kristine D Gu, Sara J Cromer, Julie M Paik, Katsiaryna Bykov, Ion Hobai, Christopher C Thompson, Deborah J Wexler, Elisabetta Patorno
Journal: BMJ (2024)

Abstract Objective To assess whether use of glucagon-like peptide-1 (GLP-1) receptor agonists before upper gastrointestinal endoscopy is associated with increased risk of pulmonary aspiration or discontinuation of the procedure compared with sodium-glucose cotransporter-2 (SGLT-2) inhibitors. Design Cohort study. Setting Two deidentified US commercial healthcare databases. Participants 43 365 adults (≥18 years) with type 2 diabetes who used a GLP-1 receptor agonist or SGLT-2 inhibitor within 30 days before upper gastrointestinal endoscopy. Main outcome measures The primary outcome was pulmonary aspiration on the day of or the day after endoscopy, defined using diagnostic codes. The secondary outcome was discontinuation of endoscopy. Risk ratios and corresponding 95% confidence intervals (CIs) were estimated after fine stratification weighting based on propensity score. Results After weighting, 24 817 adults used a GLP-1 receptor agonist (mean age 59.9 years; 63.6% female) and 18 537 used an SGLT-2 inhibitor (59.8 years; 63.7% female). Among users of GLP-1 receptor agonists and SGLT-2 inhibitors, the weighted risk per 1000 people was, respectively, 4.15 and 4.26 for pulmonary aspiration and 9.79 and 4.91 for discontinuation of endoscopy. Compared with SGLT-2 inhibitor use, GLP-1 receptor agonist use was not associated with an increased risk of pulmonary aspiration (pooled risk ratio 0.98, 95% CI 0.73 to 1.31), although it was associated with a higher risk for discontinuation of endoscopy (1.99, 1.56 to 2.53). Conclusions In this comparative cohort study, no increased risk of pulmonary aspiration during upper gastrointestinal endoscopy was observed among adults with type 2 diabetes using GLP-1 receptor agonists compared with SGLT-2 inhibitors within 30 days of the procedure; however, GLP-1 receptor agonists were associated with a higher risk of discontinuation of endoscopy, possibly owing to a higher risk of retained gastric content. In the absence of evidence from randomized trials, these findings could inform future practice recommendations on the preprocedural protocol for patients requiring endoscopy.
Adipocyte-derived glutathione promotes obesity-related breast cancer by regulating the SCARB2-ARF1-mTORC1 complex
Authors: Chenxi Zhao, Tingting Zhang, Si-Tu Xue, Peitao Zhang, Feng Wang, Yunxuan Li, Ying Liu, Luyao Zhao, Jie Wu, Yechao Yan, Xiaoyun Mao, Yuping Chen, Jian Yuan, Zhuorong Li, Ke Li
Journal: Cell Metabolism (2024)