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regeneration  (ATCC)


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    ATCC regeneration
    Regeneration, supplied by ATCC, used in various techniques. Bioz Stars score: 95/100, based on 108 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/regeneration/product/ATCC
    Average 95 stars, based on 108 article reviews
    regeneration - by Bioz Stars, 2026-02
    95/100 stars

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    (A) Wild-type spermatogonia achieve <t>regeneration</t> through a SPRY4-controlled signaling transition. At BU-D2, SPRY4 imposes repression to RTK signaling, inactivating both MAPK/ERK pathway and mTORC1, and poises the surviving A undiff spermatogonia in quiescent state. By BU-D10, MAPK/ERK pathway is released to activate ERK1/2 in the cytoplasm of A undiff spermatogonia, which then function as a major activator of mTORC1. Activated mTORC1 promotes A undiff spermatogonia transition from quiescent to cell-cycle-activated phase (proliferation) and initiates regeneration. (B) In Spry4 G-KO spermatogonia, both ERK1/2 and mTORC1 are activated in the cytoplasm of the surviving A undiff spermatogonia immediately after damage (BU-D2), resulting in rapid proliferation in response to injury. By BU-D10, hyperactivated ERK1/2 locates to the nucleus of A undiff spermatogonia and promotes fate commitment, suspending A undiff spermatogonia proliferation with inactivated mTORC1. Q, quiescent A undiff spermatogonia; A, activated A undiff spermatogonia; P, fate-primed spermatogonia; PD, PD0325901; RAPA, Rapamycin.
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    (A) Wild-type spermatogonia achieve regeneration through a SPRY4-controlled signaling transition. At BU-D2, SPRY4 imposes repression to RTK signaling, inactivating both MAPK/ERK pathway and mTORC1, and poises the surviving A undiff spermatogonia in quiescent state. By BU-D10, MAPK/ERK pathway is released to activate ERK1/2 in the cytoplasm of A undiff spermatogonia, which then function as a major activator of mTORC1. Activated mTORC1 promotes A undiff spermatogonia transition from quiescent to cell-cycle-activated phase (proliferation) and initiates regeneration. (B) In Spry4 G-KO spermatogonia, both ERK1/2 and mTORC1 are activated in the cytoplasm of the surviving A undiff spermatogonia immediately after damage (BU-D2), resulting in rapid proliferation in response to injury. By BU-D10, hyperactivated ERK1/2 locates to the nucleus of A undiff spermatogonia and promotes fate commitment, suspending A undiff spermatogonia proliferation with inactivated mTORC1. Q, quiescent A undiff spermatogonia; A, activated A undiff spermatogonia; P, fate-primed spermatogonia; PD, PD0325901; RAPA, Rapamycin.

    Journal: bioRxiv

    Article Title: Restoration of Spermatogenesis is Dependent on Activation of a SPRY4-ERK Checkpoint Following Germline Stem Cell Damage

    doi: 10.1101/2025.10.12.681919

    Figure Lengend Snippet: (A) Wild-type spermatogonia achieve regeneration through a SPRY4-controlled signaling transition. At BU-D2, SPRY4 imposes repression to RTK signaling, inactivating both MAPK/ERK pathway and mTORC1, and poises the surviving A undiff spermatogonia in quiescent state. By BU-D10, MAPK/ERK pathway is released to activate ERK1/2 in the cytoplasm of A undiff spermatogonia, which then function as a major activator of mTORC1. Activated mTORC1 promotes A undiff spermatogonia transition from quiescent to cell-cycle-activated phase (proliferation) and initiates regeneration. (B) In Spry4 G-KO spermatogonia, both ERK1/2 and mTORC1 are activated in the cytoplasm of the surviving A undiff spermatogonia immediately after damage (BU-D2), resulting in rapid proliferation in response to injury. By BU-D10, hyperactivated ERK1/2 locates to the nucleus of A undiff spermatogonia and promotes fate commitment, suspending A undiff spermatogonia proliferation with inactivated mTORC1. Q, quiescent A undiff spermatogonia; A, activated A undiff spermatogonia; P, fate-primed spermatogonia; PD, PD0325901; RAPA, Rapamycin.

    Article Snippet: To induce regeneration, busulfan (HY-B0245, MedChemExpress) was administered to mice by IP injection at a single dose of 10 mg/kg of body weight.

    Techniques: