You will be shown a scientific claim, and the abstract of a biomedical research paper. Each sentence from the abstract will be on a separate line. Your task is to return a JSON object with two fields:

- "verdict": The fact-checking verdict. If the information in the abstract supports the claim, write "SUPPORT". If the abstract contradicts the claim, write "CONTRADICT". If the abstract does not provide enough information to arrive at a verdict, write "NEI" (for "not enough information").
- "evidence": An array of sentences providing evidence for the verdict. Please copy all relevant sentences verbatim from the abstract. If the verdict was "NEI", then return an empty array.

For instance, if the model were given the claim "smoking causes cancer", the output might be
{
  "verdict": "SUPPORT",
  "evidence": ["The results of our meta-analysis provide overwhelming support that cigarette smoking is a risk cause for lung cancer."]
}

Your response should not include any text other than the json.

Claim: MICAL redox enzymes regulate actin dynamics in many cell types.

Abstract:
The Drosophila melanogaster MICAL protein is essential for the neuronal growth cone machinery that functions through plexin- and semaphorin-mediated axonal signaling.
Drosophila MICAL is also involved in regulating myofilament organization and synaptic structures, and serves as an actin disassembly factor downstream of plexin-mediated axonal repulsion.
In mammalian cells there are three known isoforms, MICAL1, MICAL2 and MICAL3, as well as the MICAL-like proteins MICAL-L1 and MICAL-L2, but little is known of their function, and information comes almost exclusively from neural cells.
In this study we show that in non-neural cells human MICALs are required for normal actin organization, and all three MICALs regulate actin stress fibers.
Moreover, we provide evidence that the generation of reactive oxygen species by MICAL proteins is crucial for their actin-regulatory function.
However, although MICAL1 is auto-inhibited by its C-terminal coiled-coil region, MICAL2 remains constitutively active and affects stress fibers.
These data suggest differential but complementary roles for MICAL1 and MICAL2 in actin microfilament regulation.
{"verdict": "SUPPORT", "evidence": ["In this study we show that in non-neural cells human MICALs are required for normal actin organization, and all three MICALs regulate actin stress fibers."]}