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  1. Article ; Online: Pancreatic β-cell mRNA modification as a marker for type 2 diabetes.

    Renström, Erik / Zhang, Enming

    Nature metabolism

    2019  Volume 1, Issue 8, Page(s) 748–749

    Language English
    Publishing date 2019-09-02
    Publishing country Germany
    Document type Journal Article
    ISSN 2522-5812
    ISSN (online) 2522-5812
    DOI 10.1038/s42255-019-0096-x
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  2. Article: The Calcium Channel Subunit Gamma-4 as a Novel Regulator of MafA in Pancreatic Beta-Cell Controls Glucose Homeostasis.

    Wu, Rui / Karagiannopoulos, Alexandros / Eliasson, Lena / Renström, Erik / Luan, Cheng / Zhang, Enming

    Biomedicines

    2022  Volume 10, Issue 4

    Abstract: Impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) are high-risk factors of diabetes development and may be caused by defective insulin secretion in pancreatic beta-cells. Glucose-stimulated insulin secretion is mediated by voltage-gated ...

    Abstract Impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) are high-risk factors of diabetes development and may be caused by defective insulin secretion in pancreatic beta-cells. Glucose-stimulated insulin secretion is mediated by voltage-gated Ca
    Language English
    Publishing date 2022-03-25
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2720867-9
    ISSN 2227-9059
    ISSN 2227-9059
    DOI 10.3390/biomedicines10040770
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  3. Article ; Online: Response to Jentsch et al.

    Renström, Erik

    Cell metabolism

    2010  Volume 12, Issue 4, Page(s) 309

    Language English
    Publishing date 2010-10-06
    Publishing country United States
    Document type Letter
    ZDB-ID 2176834-1
    ISSN 1932-7420 ; 1550-4131
    ISSN (online) 1932-7420
    ISSN 1550-4131
    DOI 10.1016/j.cmet.2010.09.003
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6169: Show issues Location:
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  4. Article ; Online: Upper-extremity Spasticity-reducing Treatment in Adjunct to Movement Training and Orthoses in Children with Cerebral Palsy at Gross Motor Function- and Manual Ability Classification System Levels IV-V: A Descriptive Study.

    Andersson, Gerd / Renström, Barbro / Blaszczyk, Izabela / Domellöf, Erik

    Developmental neurorehabilitation

    2019  Volume 23, Issue 6, Page(s) 349–358

    Abstract: Covering a 20-year period of work with children with severe cerebral palsy (CP) within a Swedish habilitation service, changes in passive wrist extension with fingers extended (PWE-FE) and current hand function are described and compared between children ...

    Abstract Covering a 20-year period of work with children with severe cerebral palsy (CP) within a Swedish habilitation service, changes in passive wrist extension with fingers extended (PWE-FE) and current hand function are described and compared between children receiving systematic upper-extremity treatment with botulinum neurotoxin type A and intervention programs from before 7 years of age (Group 1, n = 7), those whom for various reasons did not undergo this treatment (Group 2, n = 10), and those not having the option to receive treatment until later during childhood/adolescence (Group 3, n = 8). Group 3 showed more critical and less normal PWE-FE values for both wrists, and poorer hand function scores, particularly compared with Group 1. Findings cautiously suggest that repeated upper-extremity spasticity-reducing treatment and movement training/orthoses from an early age may help prevent critical loss of passive range of motion of the wrist joint flexion/extension and promote hand function development in children with severe CP.
    MeSH term(s) Botulinum Toxins, Type A/administration & dosage ; Botulinum Toxins, Type A/therapeutic use ; Cerebral Palsy/pathology ; Cerebral Palsy/rehabilitation ; Cerebral Palsy/therapy ; Child ; Child, Preschool ; Combined Modality Therapy ; Exercise Therapy/methods ; Female ; Hand/physiopathology ; Humans ; Injections, Intramuscular ; Male ; Movement ; Muscle Spasticity ; Neurological Rehabilitation/methods ; Neuromuscular Agents/administration & dosage ; Neuromuscular Agents/therapeutic use ; Orthotic Devices ; Severity of Illness Index
    Chemical Substances Neuromuscular Agents ; Botulinum Toxins, Type A (EC 3.4.24.69)
    Language English
    Publishing date 2019-08-22
    Publishing country England
    Document type Journal Article
    ZDB-ID 2280007-4
    ISSN 1751-8431 ; 1751-8423
    ISSN (online) 1751-8431
    ISSN 1751-8423
    DOI 10.1080/17518423.2019.1655677
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5416: Show issues Location:
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    Jg. 1995 - 2021: Lesesall (2.OG)
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  5. Article ; Online: Intracellular cytosolic complement component C3 regulates cytoprotective autophagy in pancreatic beta cells by interaction with ATG16L1.

    King, Ben C / Renström, Erik / Blom, Anna M

    Autophagy

    2019  Volume 15, Issue 5, Page(s) 919–921

    Abstract: Complement component C3 is central to the complement system, a humoral effector mechanism of innate immune defense. When activated, C3 covalently binds to target particles, marking them for uptake and clearance by phagocytosis. We now show that C3 also ... ...

    Abstract Complement component C3 is central to the complement system, a humoral effector mechanism of innate immune defense. When activated, C3 covalently binds to target particles, marking them for uptake and clearance by phagocytosis. We now show that C3 also exists within the cytosol where it interacts with ATG16L1, and is therefore involved in the intracellular clearance and recycling of material by macroautophagy/autophagy in pancreatic beta cells. C3 is highly expressed in isolated human islets, and its expression is upregulated in islets isolated from diabetic patients and rodents, and correlates with patient HBA1c and body mass index (BMI). Knockout of C3 in clonal beta cells leads to dysfunctional autophagy, and increased cell death after challenge with diabetogenic stresses, which are usually alleviated by increased autophagic turnover. However, autophagic degradation of INS (insulin) granules regulates total INS content, and increased autophagy due to C3 upregulation may deplete beta cell INS stores. C3 is therefore required for efficient autophagic turnover in beta cells, and is upregulated as a cytoprotective factor during diabetes.
    MeSH term(s) Animals ; Autophagy/physiology ; Autophagy-Related Proteins/metabolism ; Cells, Cultured ; Complement C3/metabolism ; Complement C3/physiology ; Cytoplasm/metabolism ; Cytoprotection/genetics ; Cytosol/metabolism ; Diabetes Mellitus/genetics ; Diabetes Mellitus/metabolism ; Diabetes Mellitus/pathology ; Gene Knockdown Techniques ; Humans ; Insulin/metabolism ; Insulin-Secreting Cells/pathology ; Insulin-Secreting Cells/physiology ; Protein Binding ; Rats
    Chemical Substances ATG16L1 protein, human ; Autophagy-Related Proteins ; Complement C3 ; Insulin
    Language English
    Publishing date 2019-02-20
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2454135-7
    ISSN 1554-8635 ; 1554-8627
    ISSN (online) 1554-8635
    ISSN 1554-8627
    DOI 10.1080/15548627.2019.1580515
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6741: Show issues Location:
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  6. Article ; Online: The T-type calcium channel Ca

    Barghouth, Mohammad / Ye, Yingying / Karagiannopoulos, Alexandros / Ma, Yunhan / Cowan, Elaine / Wu, Rui / Eliasson, Lena / Renström, Erik / Luan, Cheng / Zhang, Enming

    Cell calcium

    2022  Volume 108, Page(s) 102669

    Abstract: Voltage-gated ... ...

    Abstract Voltage-gated Ca
    MeSH term(s) Humans ; Calcium/metabolism ; Calcium Channels, L-Type/genetics ; Calcium Channels, L-Type/metabolism ; Calcium Channels, T-Type/genetics ; Calcium Channels, T-Type/metabolism ; Glucose/metabolism ; Insulin/metabolism ; Insulin Secretion ; Insulin-Secreting Cells/metabolism
    Chemical Substances Calcium (SY7Q814VUP) ; Calcium Channels, L-Type ; Calcium Channels, T-Type ; Glucose (IY9XDZ35W2) ; Insulin ; CACNA1H protein, human
    Language English
    Publishing date 2022-10-31
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 757687-0
    ISSN 1532-1991 ; 0143-4160
    ISSN (online) 1532-1991
    ISSN 0143-4160
    DOI 10.1016/j.ceca.2022.102669
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    Zs.A 1596: Show issues Location:
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  7. Article: Reduced volume of diabetic pancreatic islets in rodents detected by synchrotron X-ray phase-contrast microtomography and deep learning network.

    Guo, Qingqing / AlKendi, Abdulla / Jiang, Xiaoping / Mittone, Alberto / Wang, Linbo / Larsson, Emanuel / Bravin, Alberto / Renström, Erik / Fang, Xianyong / Zhang, Enming

    Heliyon

    2023  Volume 9, Issue 2, Page(s) e13081

    Abstract: The pancreatic islet is a highly structured micro-organ that produces insulin in response to rising blood glucose. Here we develop a label-free and automatic imaging approach to visualize the ... ...

    Abstract The pancreatic islet is a highly structured micro-organ that produces insulin in response to rising blood glucose. Here we develop a label-free and automatic imaging approach to visualize the islets
    Language English
    Publishing date 2023-01-19
    Publishing country England
    Document type Journal Article
    ZDB-ID 2835763-2
    ISSN 2405-8440
    ISSN 2405-8440
    DOI 10.1016/j.heliyon.2023.e13081
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  8. Article ; Online: The Calcium Channel Subunit Gamma-4 as a Novel Regulator of MafA in Pancreatic Beta-Cell Controls Glucose Homeostasis

    Rui Wu / Alexandros Karagiannopoulos / Lena Eliasson / Erik Renström / Cheng Luan / Enming Zhang

    Biomedicines, Vol 10, Iss 770, p

    2022  Volume 770

    Abstract: Impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) are high-risk factors of diabetes development and may be caused by defective insulin secretion in pancreatic beta-cells. Glucose-stimulated insulin secretion is mediated by voltage-gated ...

    Abstract Impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) are high-risk factors of diabetes development and may be caused by defective insulin secretion in pancreatic beta-cells. Glucose-stimulated insulin secretion is mediated by voltage-gated Ca 2+ (Ca V ) channels in which the gamma-4 subunit (Ca V γ4) is required for the beta-cell to maintain its differentiated state. We here aim to explore the involvement of Ca V γ4 in controlling glucose homeostasis by employing the Ca V γ4 −/− mice to study in vivo glucose-metabolism-related phenotypes and glucose-stimulated insulin secretion, and to investigate the underlying mechanisms. We show that Ca V γ4 −/− mice exhibit perturbed glucose homeostasis, including IFG and IGT. Glucose-stimulated insulin secretion is blunted in Ca V γ4 −/− mouse islets. Remarkably, Ca V γ4 deletion results in reduced expression of the transcription factor essential for beta-cell maturation, MafA, on both mRNA and protein levels in islets from human donors and Ca V γ4 −/− mice, as well as in INS-1 832/13 cells. Moreover, we prove that CaMKII is responsible for mediating this regulatory pathway linked between Ca V γ4 and MafA, which is further confirmed by human islet RNA-seq data. We demonstrate that Ca V γ4 is a key player in preserving normal blood glucose homeostasis, which sheds light on Ca V γ4 as a novel target for the treatment of prediabetes through correcting the impaired metabolic status.
    Keywords beta-cell ; calcium channel subunit gamma-4 ; Cacng4 ; IFG ; IGT ; MafA ; Biology (General) ; QH301-705.5
    Subject code 333
    Language English
    Publishing date 2022-03-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  9. Article ; Online: MAFA and MAFB regulate exocytosis-related genes in human β-cells.

    Cataldo, Luis Rodrigo / Singh, Tania / Achanta, Kavya / Bsharat, Sara / Prasad, Rashmi B / Luan, Cheng / Renström, Erik / Eliasson, Lena / Artner, Isabella

    Acta physiologica (Oxford, England)

    2022  Volume 234, Issue 2, Page(s) e13761

    Abstract: Aims: Reduced expression of exocytotic genes is associated with functional defects in insulin exocytosis contributing to impaired insulin secretion and type 2 diabetes (T2D) development. MAFA and MAFB transcription factors regulate β-cell physiology, ... ...

    Abstract Aims: Reduced expression of exocytotic genes is associated with functional defects in insulin exocytosis contributing to impaired insulin secretion and type 2 diabetes (T2D) development. MAFA and MAFB transcription factors regulate β-cell physiology, and their gene expression is reduced in T2D β cells. We investigate if loss of MAFA and MAFB in human β cells contributes to T2D progression by regulating genes required for insulin exocytosis.
    Methods: Three approaches were performed: (1) RNAseq analysis with the focus on exocytosis-related genes in MafA
    Results: The expression of 30 exocytosis-related genes was significantly downregulated in MafA
    Conclusion: Our data indicate that STXBP1 and STX1A are important MAFA/B-regulated exocytosis genes which may contribute to insulin exocytosis defects observed in MAFA-deficient human T2D β cells.
    MeSH term(s) Animals ; Diabetes Mellitus, Type 2/genetics ; Diabetes Mellitus, Type 2/metabolism ; Exocytosis ; Humans ; Insulin/metabolism ; Insulin Secretion ; Insulin-Secreting Cells/metabolism ; Maf Transcription Factors, Large/genetics ; Maf Transcription Factors, Large/metabolism ; MafB Transcription Factor/genetics ; MafB Transcription Factor/metabolism ; Mice
    Chemical Substances Insulin ; MAFB protein, human ; Maf Transcription Factors, Large ; MafB Transcription Factor ; Mafa protein, mouse ; Mafb protein, mouse
    Language English
    Publishing date 2022-01-11
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2218636-0
    ISSN 1748-1716 ; 1748-1708
    ISSN (online) 1748-1716
    ISSN 1748-1708
    DOI 10.1111/apha.13761
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    Uc I Zs 229: Show issues Location:
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  10. Article ; Online: GPR162 is a beta cell CART receptor.

    Lindqvist, Andreas / Abels, Mia / Shcherbina, Liliya / Ngara, Mtakai / Kryvokhyzha, Dmytro / Chriett, Sabrina / Riva, Matteo / Fajul, Abul / Barghouth, Mohammad / Luan, Cheng / Eliasson, Lena / Larsen, Olav / Rosenkilde, Mette M / Zhang, Enming / Renström, Erik / Wierup, Nils

    iScience

    2023  Volume 26, Issue 12, Page(s) 108416

    Abstract: Cocaine and amphetamine-regulated transcript (CART) is expressed in pancreatic islet cells and neuronal elements. We have previously established insulinotropic actions of CART in human and rodent islets. The receptor for CART in the pancreatic beta cells ...

    Abstract Cocaine and amphetamine-regulated transcript (CART) is expressed in pancreatic islet cells and neuronal elements. We have previously established insulinotropic actions of CART in human and rodent islets. The receptor for CART in the pancreatic beta cells is unidentified. We used RNA sequencing of
    Language English
    Publishing date 2023-11-10
    Publishing country United States
    Document type Journal Article
    ISSN 2589-0042
    ISSN (online) 2589-0042
    DOI 10.1016/j.isci.2023.108416
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